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ck2 inhibitor silmitasertib cx 4945  (MedChemExpress)


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    MedChemExpress ck2 inhibitor silmitasertib cx 4945
    Ck2 Inhibitor Silmitasertib Cx 4945, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ck2+inhibitor+silmitasertib+cx+4945/DMAT/pm40929057-87-22-29
    Average 95 stars, based on 21 article reviews
    ck2 inhibitor silmitasertib cx 4945 - by Bioz Stars, 2026-10
    95/100 stars

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    Related Articles

    Knockdown:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Infection:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Immunofluorescence:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Comparison:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Recombinant:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Concentration Assay:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Immunoprecipitation:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Liquid Chromatography with Mass Spectroscopy:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Cell Culture:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Negative Control:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Incubation:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Immunostaining:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Transfection:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Expressing:

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli-induced meningitis.
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R

    Article Title: CK2 derived from brain microvascular endothelial cells induces astrocyte inflammatory response in Escherichia coli -induced meningitis
    Article Snippet: The NF-κB inhibitor BAY11–7082, the JAK/STAT inhibitor Ruxolitinib, the JNK inhibitor SP600125, the PI3K-Akt inhibitor Wortmannin, the ERK1/2 inhibitor U0126, and the CK2 inhibitor Silmitasertib (CX-4945) were purchased from MedChem Express (Monmouth, USA). .. R



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    (A) Kinase-substrate enrichment analysis (KSEA) was performed based on phosphoproteomic data in ESCC. Kinases are considered hyper-activated when enrichment score > 0 (red) and P < 0.05, while they are regarded as inhibited when the enrichment score < 0 (blue) and P < 0.05. (B) KEGG pathway enrichment analysis results are shown for differential phosphoproteins. Pathways enriched in the upregulated ( n = 1,038) and down-regulated ( n = 574) phosphoproteins are indicated by pink and blue bars, respectively. (C) Fold change (FC) in the abundance of phosphosites conforming to the <t>CK2</t> consensus motif (S/T X X E/D) is shown (BH adjusted P value < 0.01) (D) The abundance of p-SF3B3 (T1200) in ESCC tumor (T) and adjacent normal (N) tissues ( n = 21). (E) Kaplan–Meier plots of Disease-Free Survival (DFS) in ESCC patients of p-SF3B3 (T1200). (F) The amino acid sequences surrounding T1200 in SF3B3 in different species are shown. The consensus motif for CK2 phosphorylation is shown at the bottom. (G) The specificity of p-SF3B3 (T1200) antibody was examined by using both wild-type (WT, EELDRTPPEVS) and p-T1200 (EELDRT(p)PPEVS) peptides. (H) Bacterially expressed, purified His-SF3B3 (WT) and His-SF3B3 (T1200A) proteins were examined by Coomassie blue staining (C.B.S) and indicated by the red arrow. (I) In vitro phosphorylation assay was performed by mixing bacterially expressed, purified His-SF3B3 (WT) or His-SF3B3 (T1200A) with or without CK2 kinase, followed by immunoblotting (IB) analysis using antibodies as indicated or Ponceau Staining (P.S). (J) KYSE140 cells treated with or <t>without</t> <t>CX-4945</t> (10 μM, 24 h) were subjected to immunoprecipitation (IP) with anti-SF3B3 antibody, followed by IB analysis with antibodies as indicated. (K) HEK293T cells were transfected with GFP-tagged SF3B3 and then treated with or without CX-4945 (10 μM, 24 h), followed by IP analysis with anti-GFP antibody and IB analysis with antibodies as indicated. (L) KYSE140 cells were subjected to IP analysis with control IgG or anti-SF3B3 antibody, followed by IB analysis with antibodies as indicated. (M) HEK293T cells transfected with FLAG-tagged CSNK2A1 and GFP-tagged SF3B3 were subjected to IP analysis with anti-Flag M2 agarose, followed by IB analysis with antibodies as indicated. (N) HEK293T cells transfected with FLAG-tagged SF3B3 and MYC-tagged CSNK2A1 were subjected to IP analysis with anti-Flag M2 agarose, followed by IB analysis with antibodies as indicated. The data underlying the graphs shown can be found in .
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    (A) Kinase-substrate enrichment analysis (KSEA) was performed based on phosphoproteomic data in ESCC. Kinases are considered hyper-activated when enrichment score > 0 (red) and P < 0.05, while they are regarded as inhibited when the enrichment score < 0 (blue) and P < 0.05. (B) KEGG pathway enrichment analysis results are shown for differential phosphoproteins. Pathways enriched in the upregulated ( n = 1,038) and down-regulated ( n = 574) phosphoproteins are indicated by pink and blue bars, respectively. (C) Fold change (FC) in the abundance of phosphosites conforming to the <t>CK2</t> consensus motif (S/T X X E/D) is shown (BH adjusted P value < 0.01) (D) The abundance of p-SF3B3 (T1200) in ESCC tumor (T) and adjacent normal (N) tissues ( n = 21). (E) Kaplan–Meier plots of Disease-Free Survival (DFS) in ESCC patients of p-SF3B3 (T1200). (F) The amino acid sequences surrounding T1200 in SF3B3 in different species are shown. The consensus motif for CK2 phosphorylation is shown at the bottom. (G) The specificity of p-SF3B3 (T1200) antibody was examined by using both wild-type (WT, EELDRTPPEVS) and p-T1200 (EELDRT(p)PPEVS) peptides. (H) Bacterially expressed, purified His-SF3B3 (WT) and His-SF3B3 (T1200A) proteins were examined by Coomassie blue staining (C.B.S) and indicated by the red arrow. (I) In vitro phosphorylation assay was performed by mixing bacterially expressed, purified His-SF3B3 (WT) or His-SF3B3 (T1200A) with or without CK2 kinase, followed by immunoblotting (IB) analysis using antibodies as indicated or Ponceau Staining (P.S). (J) KYSE140 cells treated with or <t>without</t> <t>CX-4945</t> (10 μM, 24 h) were subjected to immunoprecipitation (IP) with anti-SF3B3 antibody, followed by IB analysis with antibodies as indicated. (K) HEK293T cells were transfected with GFP-tagged SF3B3 and then treated with or without CX-4945 (10 μM, 24 h), followed by IP analysis with anti-GFP antibody and IB analysis with antibodies as indicated. (L) KYSE140 cells were subjected to IP analysis with control IgG or anti-SF3B3 antibody, followed by IB analysis with antibodies as indicated. (M) HEK293T cells transfected with FLAG-tagged CSNK2A1 and GFP-tagged SF3B3 were subjected to IP analysis with anti-Flag M2 agarose, followed by IB analysis with antibodies as indicated. (N) HEK293T cells transfected with FLAG-tagged SF3B3 and MYC-tagged CSNK2A1 were subjected to IP analysis with anti-Flag M2 agarose, followed by IB analysis with antibodies as indicated. The data underlying the graphs shown can be found in .
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    ck2 inhibitor cx-4945 (silmitasertib)  (ApexBio)
    90
    ApexBio ck2 inhibitor cx-4945 (silmitasertib)
    (A) Kinase-substrate enrichment analysis (KSEA) was performed based on phosphoproteomic data in ESCC. Kinases are considered hyper-activated when enrichment score > 0 (red) and P < 0.05, while they are regarded as inhibited when the enrichment score < 0 (blue) and P < 0.05. (B) KEGG pathway enrichment analysis results are shown for differential phosphoproteins. Pathways enriched in the upregulated ( n = 1,038) and down-regulated ( n = 574) phosphoproteins are indicated by pink and blue bars, respectively. (C) Fold change (FC) in the abundance of phosphosites conforming to the <t>CK2</t> consensus motif (S/T X X E/D) is shown (BH adjusted P value < 0.01) (D) The abundance of p-SF3B3 (T1200) in ESCC tumor (T) and adjacent normal (N) tissues ( n = 21). (E) Kaplan–Meier plots of Disease-Free Survival (DFS) in ESCC patients of p-SF3B3 (T1200). (F) The amino acid sequences surrounding T1200 in SF3B3 in different species are shown. The consensus motif for CK2 phosphorylation is shown at the bottom. (G) The specificity of p-SF3B3 (T1200) antibody was examined by using both wild-type (WT, EELDRTPPEVS) and p-T1200 (EELDRT(p)PPEVS) peptides. (H) Bacterially expressed, purified His-SF3B3 (WT) and His-SF3B3 (T1200A) proteins were examined by Coomassie blue staining (C.B.S) and indicated by the red arrow. (I) In vitro phosphorylation assay was performed by mixing bacterially expressed, purified His-SF3B3 (WT) or His-SF3B3 (T1200A) with or without CK2 kinase, followed by immunoblotting (IB) analysis using antibodies as indicated or Ponceau Staining (P.S). (J) KYSE140 cells treated with or <t>without</t> <t>CX-4945</t> (10 μM, 24 h) were subjected to immunoprecipitation (IP) with anti-SF3B3 antibody, followed by IB analysis with antibodies as indicated. (K) HEK293T cells were transfected with GFP-tagged SF3B3 and then treated with or without CX-4945 (10 μM, 24 h), followed by IP analysis with anti-GFP antibody and IB analysis with antibodies as indicated. (L) KYSE140 cells were subjected to IP analysis with control IgG or anti-SF3B3 antibody, followed by IB analysis with antibodies as indicated. (M) HEK293T cells transfected with FLAG-tagged CSNK2A1 and GFP-tagged SF3B3 were subjected to IP analysis with anti-Flag M2 agarose, followed by IB analysis with antibodies as indicated. (N) HEK293T cells transfected with FLAG-tagged SF3B3 and MYC-tagged CSNK2A1 were subjected to IP analysis with anti-Flag M2 agarose, followed by IB analysis with antibodies as indicated. The data underlying the graphs shown can be found in .
    Ck2 Inhibitor Cx 4945 (Silmitasertib), supplied by ApexBio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ck2 inhibitor cx 4945  (Selleck Chemicals)
    93
    Selleck Chemicals ck2 inhibitor cx 4945
    (A) Exposure-matched epifluorescent images for CK2α, G3BP1, and G3BP1PS149 in DRGs transfected with Cnsk2a1/2 (siCsnk2a1/2) and control (siCon) siRNAs.
    Ck2 Inhibitor Cx 4945, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    (A) Kinase-substrate enrichment analysis (KSEA) was performed based on phosphoproteomic data in ESCC. Kinases are considered hyper-activated when enrichment score > 0 (red) and P < 0.05, while they are regarded as inhibited when the enrichment score < 0 (blue) and P < 0.05. (B) KEGG pathway enrichment analysis results are shown for differential phosphoproteins. Pathways enriched in the upregulated ( n = 1,038) and down-regulated ( n = 574) phosphoproteins are indicated by pink and blue bars, respectively. (C) Fold change (FC) in the abundance of phosphosites conforming to the CK2 consensus motif (S/T X X E/D) is shown (BH adjusted P value < 0.01) (D) The abundance of p-SF3B3 (T1200) in ESCC tumor (T) and adjacent normal (N) tissues ( n = 21). (E) Kaplan–Meier plots of Disease-Free Survival (DFS) in ESCC patients of p-SF3B3 (T1200). (F) The amino acid sequences surrounding T1200 in SF3B3 in different species are shown. The consensus motif for CK2 phosphorylation is shown at the bottom. (G) The specificity of p-SF3B3 (T1200) antibody was examined by using both wild-type (WT, EELDRTPPEVS) and p-T1200 (EELDRT(p)PPEVS) peptides. (H) Bacterially expressed, purified His-SF3B3 (WT) and His-SF3B3 (T1200A) proteins were examined by Coomassie blue staining (C.B.S) and indicated by the red arrow. (I) In vitro phosphorylation assay was performed by mixing bacterially expressed, purified His-SF3B3 (WT) or His-SF3B3 (T1200A) with or without CK2 kinase, followed by immunoblotting (IB) analysis using antibodies as indicated or Ponceau Staining (P.S). (J) KYSE140 cells treated with or without CX-4945 (10 μM, 24 h) were subjected to immunoprecipitation (IP) with anti-SF3B3 antibody, followed by IB analysis with antibodies as indicated. (K) HEK293T cells were transfected with GFP-tagged SF3B3 and then treated with or without CX-4945 (10 μM, 24 h), followed by IP analysis with anti-GFP antibody and IB analysis with antibodies as indicated. (L) KYSE140 cells were subjected to IP analysis with control IgG or anti-SF3B3 antibody, followed by IB analysis with antibodies as indicated. (M) HEK293T cells transfected with FLAG-tagged CSNK2A1 and GFP-tagged SF3B3 were subjected to IP analysis with anti-Flag M2 agarose, followed by IB analysis with antibodies as indicated. (N) HEK293T cells transfected with FLAG-tagged SF3B3 and MYC-tagged CSNK2A1 were subjected to IP analysis with anti-Flag M2 agarose, followed by IB analysis with antibodies as indicated. The data underlying the graphs shown can be found in .

    Journal: PLOS Biology

    Article Title: Casein kinase 2-mediated phosphorylation of the splicing factor SF3B3 plays a key role in esophageal squamous cell carcinoma progression

    doi: 10.1371/journal.pbio.3003729

    Figure Lengend Snippet: (A) Kinase-substrate enrichment analysis (KSEA) was performed based on phosphoproteomic data in ESCC. Kinases are considered hyper-activated when enrichment score > 0 (red) and P < 0.05, while they are regarded as inhibited when the enrichment score < 0 (blue) and P < 0.05. (B) KEGG pathway enrichment analysis results are shown for differential phosphoproteins. Pathways enriched in the upregulated ( n = 1,038) and down-regulated ( n = 574) phosphoproteins are indicated by pink and blue bars, respectively. (C) Fold change (FC) in the abundance of phosphosites conforming to the CK2 consensus motif (S/T X X E/D) is shown (BH adjusted P value < 0.01) (D) The abundance of p-SF3B3 (T1200) in ESCC tumor (T) and adjacent normal (N) tissues ( n = 21). (E) Kaplan–Meier plots of Disease-Free Survival (DFS) in ESCC patients of p-SF3B3 (T1200). (F) The amino acid sequences surrounding T1200 in SF3B3 in different species are shown. The consensus motif for CK2 phosphorylation is shown at the bottom. (G) The specificity of p-SF3B3 (T1200) antibody was examined by using both wild-type (WT, EELDRTPPEVS) and p-T1200 (EELDRT(p)PPEVS) peptides. (H) Bacterially expressed, purified His-SF3B3 (WT) and His-SF3B3 (T1200A) proteins were examined by Coomassie blue staining (C.B.S) and indicated by the red arrow. (I) In vitro phosphorylation assay was performed by mixing bacterially expressed, purified His-SF3B3 (WT) or His-SF3B3 (T1200A) with or without CK2 kinase, followed by immunoblotting (IB) analysis using antibodies as indicated or Ponceau Staining (P.S). (J) KYSE140 cells treated with or without CX-4945 (10 μM, 24 h) were subjected to immunoprecipitation (IP) with anti-SF3B3 antibody, followed by IB analysis with antibodies as indicated. (K) HEK293T cells were transfected with GFP-tagged SF3B3 and then treated with or without CX-4945 (10 μM, 24 h), followed by IP analysis with anti-GFP antibody and IB analysis with antibodies as indicated. (L) KYSE140 cells were subjected to IP analysis with control IgG or anti-SF3B3 antibody, followed by IB analysis with antibodies as indicated. (M) HEK293T cells transfected with FLAG-tagged CSNK2A1 and GFP-tagged SF3B3 were subjected to IP analysis with anti-Flag M2 agarose, followed by IB analysis with antibodies as indicated. (N) HEK293T cells transfected with FLAG-tagged SF3B3 and MYC-tagged CSNK2A1 were subjected to IP analysis with anti-Flag M2 agarose, followed by IB analysis with antibodies as indicated. The data underlying the graphs shown can be found in .

    Article Snippet: The proteasome inhibitor MG-132 (T2154), the CK2 inhibitor CX-4945 (T2259), and the USP7 inhibitor P5091 (T6925) were purchased from TargetMol.

    Techniques: Phospho-proteomics, Purification, Staining, In Vitro, Western Blot, Immunoprecipitation, Transfection, Control

    (A) KYSE140 and KYSE30 cells were treated with CX-4945 for 0, 12, and 24 h (10 μM), followed by IB analysis with antibodies as indicated. (B) KYSE30 cells were treated with CX-4945 (10 μM) for 12 h and then treated with cycloheximide (CHX) (50 μg/ml) for 0, 4, 8, or 12 h, followed by IB analysis with antibodies as indicated. (C) The quantification of SF3B3 proteins in (B) is shown (mean ± SD; * P < 0.05, Student t test). (D) KYSE30 cells were infected with lentivirus expressing SF3B3 (WT), SF3B3 (T1200A), or SF3B3 (T1200D) for 48 h and then treated with CHX (50 μg/mL) for 0, 4, 8, or 12 hours, followed by IB analysis with antibodies as indicated. (E) The quantification of SF3B3 proteins in (D) is shown (mean ± SD; * P < 0.05, ** P < 0.01, Student t test). (F) The rela t ive expression of SF3B3 in ESCC tumor (T) and adjacent normal (N) tissues (n = 124) from CPPA database is shown. (G) Kaplan–Meier plots of overall survival of SF3B3 in ESCC patients using the CPPA dataset. (H) The correlation between the expression of SF3B3 and the abundance of p-SF3B3 (T1200) in ESCC clinical samples as described in is shown. (I) The correlation between PTMSEA score of CK2 and the expression of SF3B3 in ESCC clinical samples as described in is shown. The data underlying the graphs shown can be found in .

    Journal: PLOS Biology

    Article Title: Casein kinase 2-mediated phosphorylation of the splicing factor SF3B3 plays a key role in esophageal squamous cell carcinoma progression

    doi: 10.1371/journal.pbio.3003729

    Figure Lengend Snippet: (A) KYSE140 and KYSE30 cells were treated with CX-4945 for 0, 12, and 24 h (10 μM), followed by IB analysis with antibodies as indicated. (B) KYSE30 cells were treated with CX-4945 (10 μM) for 12 h and then treated with cycloheximide (CHX) (50 μg/ml) for 0, 4, 8, or 12 h, followed by IB analysis with antibodies as indicated. (C) The quantification of SF3B3 proteins in (B) is shown (mean ± SD; * P < 0.05, Student t test). (D) KYSE30 cells were infected with lentivirus expressing SF3B3 (WT), SF3B3 (T1200A), or SF3B3 (T1200D) for 48 h and then treated with CHX (50 μg/mL) for 0, 4, 8, or 12 hours, followed by IB analysis with antibodies as indicated. (E) The quantification of SF3B3 proteins in (D) is shown (mean ± SD; * P < 0.05, ** P < 0.01, Student t test). (F) The rela t ive expression of SF3B3 in ESCC tumor (T) and adjacent normal (N) tissues (n = 124) from CPPA database is shown. (G) Kaplan–Meier plots of overall survival of SF3B3 in ESCC patients using the CPPA dataset. (H) The correlation between the expression of SF3B3 and the abundance of p-SF3B3 (T1200) in ESCC clinical samples as described in is shown. (I) The correlation between PTMSEA score of CK2 and the expression of SF3B3 in ESCC clinical samples as described in is shown. The data underlying the graphs shown can be found in .

    Article Snippet: The proteasome inhibitor MG-132 (T2154), the CK2 inhibitor CX-4945 (T2259), and the USP7 inhibitor P5091 (T6925) were purchased from TargetMol.

    Techniques: Infection, Expressing

    (A) KYSE140 cells transfected with siCTL or two independent siSF3B3 (siSF3B3-1 and siSF3B3-2) were subjected to RT-qPCR analysis to assess mRNA expression levels of SF3B3 (mean ± SD; *** P < 0.001, Student t test). (B) RNA extracted from cells as described in (A) were subjected to library preparation and Nanopore sequencing, and the number of alternative splicing (AS) events regulated by SF3B3 is shown (|ΔPSI| ≥ 0.2 and FDR ≤ 0.05). Cassette Exons or Exon Skipping (ES); Intron Retain (IR); Alternative 5′ Splice Site (5′ ASS); Alternative 3′ Splice Site (3′ ASS). (C) The number of exon inclusion and skipping induced by SF3B3 is shown by pie chart. (D) The Pearson’s correlation was analyzed between the expression levels of SF3B3 and genes containing SF3B3-regulated cassette exons that are highly expressed in ESCC (Log 2 FC ≥ 2, P ≤ 0.01). Red dots indicate genes with r ≥ 0.3. (E) GO analysis results for genes with SF3B3-regulated cassette exons. The top 6 most enriched GO terms are shown. (F) Kaplan–Meier analyses of progression-free interval in ESCC patients using EXOSC2 cassette exon 4 as an input in the OncoSplicing dataset. (G) KYSE140 cells transfected with siCTL, siSF3B3-1, or siSF3B3-2 were subjected to standard PCR analysis to examine the expression of both the short and long isoforms of EXOSC2 as indicated at the bottom. Percentage spliced in (PSI) values were measured by Image J. The position of the cassette exon in EXOSC2 is as follows: EXOSC2 ( NM_001114122 , exon 4). DNA marker is indicated on the left. (H) KYSE140 cells were transfected with siCTL or siSF3B3 in the presence or absence of control vector, SF3B3 (WT), or SF3B3 (T1200A), followed by standard PCR analysis to examine the short and long isoforms of EXOSC2 as described in (G). (I) KYSE140 cells treated with or without CX-4945 (10 μM) were subjected to standard PCR analysis to examine the short and long isoforms of EXOSC2 as described in (G). (J) HEK293T cells transfected with GFP control vector or GFP-tagged SF3B3 (WT), SF3B3 (T1200A), or SF3B3 (T1200D) were subjected to IP analysis with anti-GFP magnetic beads, followed by IB analysis with antibodies as indicated. (K) HEK293T cells transfected with GFP control vector or GFP-tagged SF3B3 (WT), SF3B3 (T1200A), or SF3B3 (T1200D) were subjected to RIP analysis with anti-GFP magnetic beads, followed by RT-qPCR analysis to examine the binding of SF3B3 protein with genes as indicated (mean ± SD; *** P < 0.001, ** P < 0.01, Student t test) . (L–N) KYSE140 cells s t ably expressing control lentiviral vector, EXOSC2 long isoform (EXOSC2-L), or EXOSC2 short isoform (EXOSC2-S) were subjected to IB analysis (L), cell proliferation assay (M), and colony formation assay (N) (mean ± SD; ns: not significant, *** P < 0.001, Student t test). (O) The quantifica t ion of the crystal violet dye in (N) is shown (mean ± SD; ns: not significant, ** P < 0.01, *** P < 0.001, Student t test). (P–R) KYSE140 cells transfected with siCTL or siSF3B3, followed by infec t ion with lentivirus expressing control vector, EXOSC2-L, or EXOSC2-S were subjected to IB analysis (P), cell proliferation assay (Q), and colony formation assay (R) (mean ± SD; * P < 0.05, ** P < 0.01, Student t test). (S) The quantification of the number of colonies in (R) (mean ± SD; *** P < 0.001, Student t test). (T) KYSE140 cells infected with lentivirus expressing shCTL or shSF3B3 in the presence or absence of lentivirus expressing control vec t or, EXOSC2-L, or EXOSC2-S were injected into BALB/c nude mice for 4 weeks, and the tumors were collected and photographed. (U, V) The tumor volume (U) and weight (V) as shown in (T) (mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001, Student t test). (W) The expression of the short and long isoforms of EXOSC2 were measured by standard PCR as described in (G) in paired ESCC and adjacent normal tissues ( n = 6). (X) The quantification of the PSI values in (W) (mean ± SD; * P < 0.05, Student t test). The data underlying the graphs shown can be found in .

    Journal: PLOS Biology

    Article Title: Casein kinase 2-mediated phosphorylation of the splicing factor SF3B3 plays a key role in esophageal squamous cell carcinoma progression

    doi: 10.1371/journal.pbio.3003729

    Figure Lengend Snippet: (A) KYSE140 cells transfected with siCTL or two independent siSF3B3 (siSF3B3-1 and siSF3B3-2) were subjected to RT-qPCR analysis to assess mRNA expression levels of SF3B3 (mean ± SD; *** P < 0.001, Student t test). (B) RNA extracted from cells as described in (A) were subjected to library preparation and Nanopore sequencing, and the number of alternative splicing (AS) events regulated by SF3B3 is shown (|ΔPSI| ≥ 0.2 and FDR ≤ 0.05). Cassette Exons or Exon Skipping (ES); Intron Retain (IR); Alternative 5′ Splice Site (5′ ASS); Alternative 3′ Splice Site (3′ ASS). (C) The number of exon inclusion and skipping induced by SF3B3 is shown by pie chart. (D) The Pearson’s correlation was analyzed between the expression levels of SF3B3 and genes containing SF3B3-regulated cassette exons that are highly expressed in ESCC (Log 2 FC ≥ 2, P ≤ 0.01). Red dots indicate genes with r ≥ 0.3. (E) GO analysis results for genes with SF3B3-regulated cassette exons. The top 6 most enriched GO terms are shown. (F) Kaplan–Meier analyses of progression-free interval in ESCC patients using EXOSC2 cassette exon 4 as an input in the OncoSplicing dataset. (G) KYSE140 cells transfected with siCTL, siSF3B3-1, or siSF3B3-2 were subjected to standard PCR analysis to examine the expression of both the short and long isoforms of EXOSC2 as indicated at the bottom. Percentage spliced in (PSI) values were measured by Image J. The position of the cassette exon in EXOSC2 is as follows: EXOSC2 ( NM_001114122 , exon 4). DNA marker is indicated on the left. (H) KYSE140 cells were transfected with siCTL or siSF3B3 in the presence or absence of control vector, SF3B3 (WT), or SF3B3 (T1200A), followed by standard PCR analysis to examine the short and long isoforms of EXOSC2 as described in (G). (I) KYSE140 cells treated with or without CX-4945 (10 μM) were subjected to standard PCR analysis to examine the short and long isoforms of EXOSC2 as described in (G). (J) HEK293T cells transfected with GFP control vector or GFP-tagged SF3B3 (WT), SF3B3 (T1200A), or SF3B3 (T1200D) were subjected to IP analysis with anti-GFP magnetic beads, followed by IB analysis with antibodies as indicated. (K) HEK293T cells transfected with GFP control vector or GFP-tagged SF3B3 (WT), SF3B3 (T1200A), or SF3B3 (T1200D) were subjected to RIP analysis with anti-GFP magnetic beads, followed by RT-qPCR analysis to examine the binding of SF3B3 protein with genes as indicated (mean ± SD; *** P < 0.001, ** P < 0.01, Student t test) . (L–N) KYSE140 cells s t ably expressing control lentiviral vector, EXOSC2 long isoform (EXOSC2-L), or EXOSC2 short isoform (EXOSC2-S) were subjected to IB analysis (L), cell proliferation assay (M), and colony formation assay (N) (mean ± SD; ns: not significant, *** P < 0.001, Student t test). (O) The quantifica t ion of the crystal violet dye in (N) is shown (mean ± SD; ns: not significant, ** P < 0.01, *** P < 0.001, Student t test). (P–R) KYSE140 cells transfected with siCTL or siSF3B3, followed by infec t ion with lentivirus expressing control vector, EXOSC2-L, or EXOSC2-S were subjected to IB analysis (P), cell proliferation assay (Q), and colony formation assay (R) (mean ± SD; * P < 0.05, ** P < 0.01, Student t test). (S) The quantification of the number of colonies in (R) (mean ± SD; *** P < 0.001, Student t test). (T) KYSE140 cells infected with lentivirus expressing shCTL or shSF3B3 in the presence or absence of lentivirus expressing control vec t or, EXOSC2-L, or EXOSC2-S were injected into BALB/c nude mice for 4 weeks, and the tumors were collected and photographed. (U, V) The tumor volume (U) and weight (V) as shown in (T) (mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001, Student t test). (W) The expression of the short and long isoforms of EXOSC2 were measured by standard PCR as described in (G) in paired ESCC and adjacent normal tissues ( n = 6). (X) The quantification of the PSI values in (W) (mean ± SD; * P < 0.05, Student t test). The data underlying the graphs shown can be found in .

    Article Snippet: The proteasome inhibitor MG-132 (T2154), the CK2 inhibitor CX-4945 (T2259), and the USP7 inhibitor P5091 (T6925) were purchased from TargetMol.

    Techniques: Transfection, Quantitative RT-PCR, Expressing, Nanopore Sequencing, Alternative Splicing, Marker, Control, Plasmid Preparation, Magnetic Beads, Binding Assay, Proliferation Assay, Colony Assay, Infection, Injection

    (A, B) KYSE140 cells were treated with CX-4945 (A) or P5091 (B) at concentrations as indicated for 72 h before cell viability measurement, and the IC50 is shown. (C, D, F, G) KYSE140 cells were treated with CX-4945 or P5091 at concentrations as indicated, followed by cell proliferation (C, F) and colony formation (D, G) assay (mean ± SD; *** P < 0.001, Student t test). (E, H) The quantification of the crystal violet dye in (D) (E) and (G) (H) is shown (mean ± SD; *** P < 0.001, Student t test). (I) An inhibitory dose-response matrix of CX-4945 and P5091 was conducted in KYSE140 cells. (J) Synergy heatmaps representing combination treatment with CX-4945 and P5091 for 3 days in KYSE140. Red color denotes drug synergy. HSA: Highest Single Agent. (K, L) KYSE140 cells were treated with CX4945 (10 μM) or P5091 (20 μM) alone or in combination followed by cell proliferation (K) and colony formation (L) assay (mean ± SD, *** P < 0.001, Student t test). (M) The quan t ification of the crystal violet dye in (L) is shown (mean ± SD, *** P < 0.001, Student t test). (N, O) KYSE140 cells were trea t ed with CX4945 (10 μM) or P5091 (20 μM) alone or in combination followed by IB analysis (N) to examine the protein levels of SF3B3 and standard PCR analysis (O) to examine the alternative splicing of EXOSC2. (P) Male BALB/c nude mice were subcutaneously injected with KYSE30 cells for 20 days and then randomized (3 mice/group) and treated with CX4945 (25 mg/kg) or P5091 (25 mg/kg) alone or in combination as indicated by intraperitoneal (i.p.) injection daily before tumor collection. (Q) Images of excised tumors in (P) are shown. (R, S) The tumor growth curve (R) and tumor weight (S) as described in (P) are shown (mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001, Student t test). The data underlying the graphs shown can be found in .

    Journal: PLOS Biology

    Article Title: Casein kinase 2-mediated phosphorylation of the splicing factor SF3B3 plays a key role in esophageal squamous cell carcinoma progression

    doi: 10.1371/journal.pbio.3003729

    Figure Lengend Snippet: (A, B) KYSE140 cells were treated with CX-4945 (A) or P5091 (B) at concentrations as indicated for 72 h before cell viability measurement, and the IC50 is shown. (C, D, F, G) KYSE140 cells were treated with CX-4945 or P5091 at concentrations as indicated, followed by cell proliferation (C, F) and colony formation (D, G) assay (mean ± SD; *** P < 0.001, Student t test). (E, H) The quantification of the crystal violet dye in (D) (E) and (G) (H) is shown (mean ± SD; *** P < 0.001, Student t test). (I) An inhibitory dose-response matrix of CX-4945 and P5091 was conducted in KYSE140 cells. (J) Synergy heatmaps representing combination treatment with CX-4945 and P5091 for 3 days in KYSE140. Red color denotes drug synergy. HSA: Highest Single Agent. (K, L) KYSE140 cells were treated with CX4945 (10 μM) or P5091 (20 μM) alone or in combination followed by cell proliferation (K) and colony formation (L) assay (mean ± SD, *** P < 0.001, Student t test). (M) The quan t ification of the crystal violet dye in (L) is shown (mean ± SD, *** P < 0.001, Student t test). (N, O) KYSE140 cells were trea t ed with CX4945 (10 μM) or P5091 (20 μM) alone or in combination followed by IB analysis (N) to examine the protein levels of SF3B3 and standard PCR analysis (O) to examine the alternative splicing of EXOSC2. (P) Male BALB/c nude mice were subcutaneously injected with KYSE30 cells for 20 days and then randomized (3 mice/group) and treated with CX4945 (25 mg/kg) or P5091 (25 mg/kg) alone or in combination as indicated by intraperitoneal (i.p.) injection daily before tumor collection. (Q) Images of excised tumors in (P) are shown. (R, S) The tumor growth curve (R) and tumor weight (S) as described in (P) are shown (mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001, Student t test). The data underlying the graphs shown can be found in .

    Article Snippet: The proteasome inhibitor MG-132 (T2154), the CK2 inhibitor CX-4945 (T2259), and the USP7 inhibitor P5091 (T6925) were purchased from TargetMol.

    Techniques: Alternative Splicing, Injection

    In ESCC, aberrantly activated CK2 phosphorylates SF3B3 at Thr1200, enhancing its interaction with the deubiquitinase USP7. This interaction leads to deubiquitination and stabilization of SF3B3, ultimately promoting a large cohort of alternative splicing events, including the inclusion of exon 4 in EXOSC2, and thereby driving ESCC progression. Targeting both CK2 and USP7, either individually or in combination, using CX-4945 and P5091, respectively, effectively suppresses ESCC progression.

    Journal: PLOS Biology

    Article Title: Casein kinase 2-mediated phosphorylation of the splicing factor SF3B3 plays a key role in esophageal squamous cell carcinoma progression

    doi: 10.1371/journal.pbio.3003729

    Figure Lengend Snippet: In ESCC, aberrantly activated CK2 phosphorylates SF3B3 at Thr1200, enhancing its interaction with the deubiquitinase USP7. This interaction leads to deubiquitination and stabilization of SF3B3, ultimately promoting a large cohort of alternative splicing events, including the inclusion of exon 4 in EXOSC2, and thereby driving ESCC progression. Targeting both CK2 and USP7, either individually or in combination, using CX-4945 and P5091, respectively, effectively suppresses ESCC progression.

    Article Snippet: The proteasome inhibitor MG-132 (T2154), the CK2 inhibitor CX-4945 (T2259), and the USP7 inhibitor P5091 (T6925) were purchased from TargetMol.

    Techniques: Alternative Splicing

    (A) Exposure-matched epifluorescent images for CK2α, G3BP1, and G3BP1PS149 in DRGs transfected with Cnsk2a1/2 (siCsnk2a1/2) and control (siCon) siRNAs.

    Journal: Current biology : CB

    Article Title: A Ca 2+ -Dependent Switch Activates Axonal Casein Kinase 2α Translation and Drives G3BP1 Granule Disassembly for Axon Regeneration

    doi: 10.1016/j.cub.2020.09.043

    Figure Lengend Snippet: (A) Exposure-matched epifluorescent images for CK2α, G3BP1, and G3BP1PS149 in DRGs transfected with Cnsk2a1/2 (siCsnk2a1/2) and control (siCon) siRNAs.

    Article Snippet: CK2 inhibitor (CX-4945) , Selleckchem , S2248.

    Techniques: Transfection, Control

    (A and B) Exposure-matched confocal images for CK2α in naive and 24 h post-injured sciatic nerve from wild-type versus mTOR 3′ UTR−/− mice shown in (A). Upper rows of image pairs show CK2α merged with NF signals in single XY planes; lower rows show XYZ projections of CK2α signals that overlap with NF (axonal CK2α) across individual XY planes. (B) shows quantitation of axonal CK2α from sciatic nerve axons as mean ± SEM (N = 3 animals; **p ≤ 0.01, ***p ≤ 0.001, and ****p ≤ 0.0001 between the indicated groups by one-way ANOVA with Tukey HSD post hoc; scale bar represents 10 μm).

    Journal: Current biology : CB

    Article Title: A Ca 2+ -Dependent Switch Activates Axonal Casein Kinase 2α Translation and Drives G3BP1 Granule Disassembly for Axon Regeneration

    doi: 10.1016/j.cub.2020.09.043

    Figure Lengend Snippet: (A and B) Exposure-matched confocal images for CK2α in naive and 24 h post-injured sciatic nerve from wild-type versus mTOR 3′ UTR−/− mice shown in (A). Upper rows of image pairs show CK2α merged with NF signals in single XY planes; lower rows show XYZ projections of CK2α signals that overlap with NF (axonal CK2α) across individual XY planes. (B) shows quantitation of axonal CK2α from sciatic nerve axons as mean ± SEM (N = 3 animals; **p ≤ 0.01, ***p ≤ 0.001, and ****p ≤ 0.0001 between the indicated groups by one-way ANOVA with Tukey HSD post hoc; scale bar represents 10 μm).

    Article Snippet: CK2 inhibitor (CX-4945) , Selleckchem , S2248.

    Techniques: Quantitation Assay

    (A) Schematic for experimental approach to test for CK2α effects on signaling to G3BP1 for axon growth.

    Journal: Current biology : CB

    Article Title: A Ca 2+ -Dependent Switch Activates Axonal Casein Kinase 2α Translation and Drives G3BP1 Granule Disassembly for Axon Regeneration

    doi: 10.1016/j.cub.2020.09.043

    Figure Lengend Snippet: (A) Schematic for experimental approach to test for CK2α effects on signaling to G3BP1 for axon growth.

    Article Snippet: CK2 inhibitor (CX-4945) , Selleckchem , S2248.

    Techniques:

    KEY RESOURCES TABLE

    Journal: Current biology : CB

    Article Title: A Ca 2+ -Dependent Switch Activates Axonal Casein Kinase 2α Translation and Drives G3BP1 Granule Disassembly for Axon Regeneration

    doi: 10.1016/j.cub.2020.09.043

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: CK2 inhibitor (CX-4945) , Selleckchem , S2248.

    Techniques: Virus, Isolation, Recombinant, Conjugation Assay, Software