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cx 4945 (MedChemExpress)

Name: cx 4945
Brand: MedChemExpress
Rating: 93 (22 reviews)

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MedChemExpress cx 4945

A) AML cell lines including both VEN-susceptible and resistant (Molm-13, Molm-13/VR, HL-60, HL-60/VR, U937), and AML PDX cells (2016-1, 2016-7) were treated with different concentrations <t>of</t> <t>CX-4945</t> and VEN alone or in combination with indicated doses for 48 h. Cell viability was assessed using WST reagent and cell viability was calculated relative to vehicle-treated cells as 100%. B) ZIP synergy scores for CX-4945 and VEN combination in different AML cell lines and PDX cells were shown. ZIP scores greater than 10 indicates ‘synergy’, and 0-10 indicate ‘additive’ activity between CX-4945 and VEN. C-D) AML cells (Molm-13, Molm-13/VR, PDX 2016-7) were treated with CX-4945 and VEN alone or in combination for 24 h and stained with Annexin V/7AAD for analyzing apoptosis by flow cytometry ( C ). Relative apoptosis was calculated by normalizing to vehicle treated cells ( D ). The data are presented as mean ± SD (n=2-4). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 by one-way ANOVA (Holm-Sidak’s multiple comparisons test) denotes statistical significance. E) AML cell lines (Molm-13, Molm-13/VR) were treated with CX-4945 and VEN alone or in combination for 24 h and the surface expression of chemoresistance markers (CD47 and CD123) was analyzed by flow cytometry. F) Schematic showing the workflow for dynamic BH3 profiling to measure drug-induced priming of BH3 peptides in AML cells. The difference in Cyt c release (%) with and without drug treatment was presented as delta priming. Created with BioRender.com . G) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides with and without CX-4945 treatment and calculated the delta priming. The data are presented as mean ± SEM (n=2) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test).

Cx 4945, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins"

Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

Journal: bioRxiv

doi: 10.64898/2025.12.24.696284

Figure Legend Snippet: A) AML cell lines including both VEN-susceptible and resistant (Molm-13, Molm-13/VR, HL-60, HL-60/VR, U937), and AML PDX cells (2016-1, 2016-7) were treated with different concentrations of CX-4945 and VEN alone or in combination with indicated doses for 48 h. Cell viability was assessed using WST reagent and cell viability was calculated relative to vehicle-treated cells as 100%. B) ZIP synergy scores for CX-4945 and VEN combination in different AML cell lines and PDX cells were shown. ZIP scores greater than 10 indicates ‘synergy’, and 0-10 indicate ‘additive’ activity between CX-4945 and VEN. C-D) AML cells (Molm-13, Molm-13/VR, PDX 2016-7) were treated with CX-4945 and VEN alone or in combination for 24 h and stained with Annexin V/7AAD for analyzing apoptosis by flow cytometry ( C ). Relative apoptosis was calculated by normalizing to vehicle treated cells ( D ). The data are presented as mean ± SD (n=2-4). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 by one-way ANOVA (Holm-Sidak’s multiple comparisons test) denotes statistical significance. E) AML cell lines (Molm-13, Molm-13/VR) were treated with CX-4945 and VEN alone or in combination for 24 h and the surface expression of chemoresistance markers (CD47 and CD123) was analyzed by flow cytometry. F) Schematic showing the workflow for dynamic BH3 profiling to measure drug-induced priming of BH3 peptides in AML cells. The difference in Cyt c release (%) with and without drug treatment was presented as delta priming. Created with BioRender.com . G) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides with and without CX-4945 treatment and calculated the delta priming. The data are presented as mean ± SEM (n=2) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test).

Techniques Used: Activity Assay, Staining, Flow Cytometry, Expressing

A) The common mechanisms that govern cellular MCL-1 levels at transcription, translation, and post-translation levels are depicted. The signaling cascade mediated through CK2, PI3K/AKT, and mTOR regulate transcription and translation of MCL-1 isoforms (L-large, S-short, ES-extra short). MCL-1L (anti-apoptotic) undergoes caspase-mediated cleavage to form pro-apoptotic shorter MCL-1 isoforms (S & ES) that can induce cellular apoptosis independent of BAX and BAK. Created using BioRender.com . B) The levels of MCL-1 isoforms (L and ES) were measured by immunoblotting in AML cell lines and PDX cells after 24h of treatment with CX-4945 and VEN alone or in combination. C) Quantification of MCL-1 transcript levels after treatment with CX-4945 and VEN alone or in combination for 24h in indicated AML cell lines and PDX cells by qRT-PCR. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. D) Immunoblotting analysis of AML cell lines (Molm-13, Molm-13/VR, U937) and PDX (2016-1, 2016-7) cells after 24h of treatment with CX-4945 and VEN alone or in combination. β-Actin was used as a loading control. Representative blots from two to three independent experiments were shown.

Figure Legend Snippet: A) The common mechanisms that govern cellular MCL-1 levels at transcription, translation, and post-translation levels are depicted. The signaling cascade mediated through CK2, PI3K/AKT, and mTOR regulate transcription and translation of MCL-1 isoforms (L-large, S-short, ES-extra short). MCL-1L (anti-apoptotic) undergoes caspase-mediated cleavage to form pro-apoptotic shorter MCL-1 isoforms (S & ES) that can induce cellular apoptosis independent of BAX and BAK. Created using BioRender.com . B) The levels of MCL-1 isoforms (L and ES) were measured by immunoblotting in AML cell lines and PDX cells after 24h of treatment with CX-4945 and VEN alone or in combination. C) Quantification of MCL-1 transcript levels after treatment with CX-4945 and VEN alone or in combination for 24h in indicated AML cell lines and PDX cells by qRT-PCR. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. D) Immunoblotting analysis of AML cell lines (Molm-13, Molm-13/VR, U937) and PDX (2016-1, 2016-7) cells after 24h of treatment with CX-4945 and VEN alone or in combination. β-Actin was used as a loading control. Representative blots from two to three independent experiments were shown.

Techniques Used: Western Blot, Quantitative RT-PCR, Control

A) Schematic depicting the treatment plan in AML patient-derived xenograft (PDX) mouse model. Similar scheme followed for cell line-derived xenograft (CDX) mice except the analysis after two-weeks of treatment. The NRG-S mice were irradiated and intravenously injected with AML cell lines Molm-13VR (0.25×10 6 cells/mouse), U937 (1×10 4 cells/mouse), and PDX 2016-7 (0.5×10 6 cells/mouse) and randomized into experimental groups (Vehicle, CX-4945, VEN, and CX+VEN Como). The drug treatment started after one week of cell transplantation and followed up for survival analysis or analysis after two-weeks of treatment (only for PDX). B-F) After two weeks of drug treatment, mice injected with PDX 2016-7 cells were sacrificed and spleen weight was recorded ( B ). The cells collected from spleens were analyzed by flow cytometry to analyze percent hCD45 positive cells ( C ). D-F) CBC analysis was performed on PDX 2016-7 mice after two-weeks of drug treatment by Hemavet analyzer. The data for B-F are presented as mean ± SD (n=7-8) and analyzed by one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 indicates statistical significance, while ‘ns’ denotes ‘not significant’. G) Immunoblotting analysis of spleen cells collected from PDX 2016-7 mice after two-weeks of treatment with CX-4945, VEN, and CX+VEN combo. The data for three different experimental animals was presented. H-J) Kaplan-Meyer survival analysis of 2016-7 PDX ( H ), Molm-13/VR CDX ( I ), and U937 CDX ( J ) mice after treatment with CX-4945, VEN and CX+VEN combo. The overall median survival (MS) days for each experimental group of PDX and CDX mice were provided next to the legend. *p<0.05, **p<0.01 and ***p<0.001 by Gehan-Breslow-Wilcoxon test indicates statistical significance.

Figure Legend Snippet: A) Schematic depicting the treatment plan in AML patient-derived xenograft (PDX) mouse model. Similar scheme followed for cell line-derived xenograft (CDX) mice except the analysis after two-weeks of treatment. The NRG-S mice were irradiated and intravenously injected with AML cell lines Molm-13VR (0.25×10 6 cells/mouse), U937 (1×10 4 cells/mouse), and PDX 2016-7 (0.5×10 6 cells/mouse) and randomized into experimental groups (Vehicle, CX-4945, VEN, and CX+VEN Como). The drug treatment started after one week of cell transplantation and followed up for survival analysis or analysis after two-weeks of treatment (only for PDX). B-F) After two weeks of drug treatment, mice injected with PDX 2016-7 cells were sacrificed and spleen weight was recorded ( B ). The cells collected from spleens were analyzed by flow cytometry to analyze percent hCD45 positive cells ( C ). D-F) CBC analysis was performed on PDX 2016-7 mice after two-weeks of drug treatment by Hemavet analyzer. The data for B-F are presented as mean ± SD (n=7-8) and analyzed by one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 indicates statistical significance, while ‘ns’ denotes ‘not significant’. G) Immunoblotting analysis of spleen cells collected from PDX 2016-7 mice after two-weeks of treatment with CX-4945, VEN, and CX+VEN combo. The data for three different experimental animals was presented. H-J) Kaplan-Meyer survival analysis of 2016-7 PDX ( H ), Molm-13/VR CDX ( I ), and U937 CDX ( J ) mice after treatment with CX-4945, VEN and CX+VEN combo. The overall median survival (MS) days for each experimental group of PDX and CDX mice were provided next to the legend. *p<0.05, **p<0.01 and ***p<0.001 by Gehan-Breslow-Wilcoxon test indicates statistical significance.

Techniques Used: Derivative Assay, Irradiation, Injection, Transplantation Assay, Flow Cytometry, Western Blot

A) AML cells from patients were surfaced stained with different fluorescent labeled antibodies and analyzed for the expression of markers for LSCs (CD34, CD38, TIM3) and chemoresistance (CD47 and CD123) by flow cytometry. B) The basal level expression of CK2α, BCL-XL, and CK2 activity (p-CK2 substrate) was measured in primary AML cells by immunoblotting analysis. C) The basal level apoptosis and viability of primary AML patient cells was assessed after 12-24h of post-thaw using Annexin V & dead cell kit for Muse cell analyzer. The patient cells with high basal level apoptosis were omitted and the ones used for further testing were highlighted using red square box. D & E) AML patient cells were treated with CX-4945 and VEN alone and in combination for 24 h and surface stained for different cell surface markers along with annexin V. The relative apoptosis in bulk cells ( D ), LSCs (CD34+CD38−) and chemoresistant (CD47+CD123-) subpopulations were calculated by normalizing the percent apoptosis in vehicle treated cells ( E ). The data are presented as mean ± SEM (n=6-7) and analyzed via one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, and ***p<0.001 considered as statistically significant.

Figure Legend Snippet: A) AML cells from patients were surfaced stained with different fluorescent labeled antibodies and analyzed for the expression of markers for LSCs (CD34, CD38, TIM3) and chemoresistance (CD47 and CD123) by flow cytometry. B) The basal level expression of CK2α, BCL-XL, and CK2 activity (p-CK2 substrate) was measured in primary AML cells by immunoblotting analysis. C) The basal level apoptosis and viability of primary AML patient cells was assessed after 12-24h of post-thaw using Annexin V & dead cell kit for Muse cell analyzer. The patient cells with high basal level apoptosis were omitted and the ones used for further testing were highlighted using red square box. D & E) AML patient cells were treated with CX-4945 and VEN alone and in combination for 24 h and surface stained for different cell surface markers along with annexin V. The relative apoptosis in bulk cells ( D ), LSCs (CD34+CD38−) and chemoresistant (CD47+CD123-) subpopulations were calculated by normalizing the percent apoptosis in vehicle treated cells ( E ). The data are presented as mean ± SEM (n=6-7) and analyzed via one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, and ***p<0.001 considered as statistically significant.

Techniques Used: Staining, Labeling, Expressing, Flow Cytometry, Activity Assay, Western Blot

Inhibition of CK2-mediated signaling through CX-4945 negatively affect cell survival pathways (PI3K/AKT/mTOR, NF-κB pathways) and anti-apoptotic proteins (MCL-1L and BCL-XL). Downregulation of anti-apoptotic BCL2 members (MCL-1L, BCL-XL) further enhance BCL-2 dependency and enhance VEN-mediated apoptosis in VR-AML cells. Overexpression of pro-apoptotic MCL-1ES isoform that can mediate mitochondrial depolarization independent of BAX/BAK contribute to potentiate VEN activity. Moreover, the transcriptome of VR-AML cells followed by CX-4945 and VEN combination treatment showed reversal of molecular gene signatures associated with VEN resistance and result in potentiated apoptosis in VR-AML cells. The signaling targeted by CX-4945 and VEN are represented by dotted lines. Created using BioRender.com .

Figure Legend Snippet: Inhibition of CK2-mediated signaling through CX-4945 negatively affect cell survival pathways (PI3K/AKT/mTOR, NF-κB pathways) and anti-apoptotic proteins (MCL-1L and BCL-XL). Downregulation of anti-apoptotic BCL2 members (MCL-1L, BCL-XL) further enhance BCL-2 dependency and enhance VEN-mediated apoptosis in VR-AML cells. Overexpression of pro-apoptotic MCL-1ES isoform that can mediate mitochondrial depolarization independent of BAX/BAK contribute to potentiate VEN activity. Moreover, the transcriptome of VR-AML cells followed by CX-4945 and VEN combination treatment showed reversal of molecular gene signatures associated with VEN resistance and result in potentiated apoptosis in VR-AML cells. The signaling targeted by CX-4945 and VEN are represented by dotted lines. Created using BioRender.com .

Techniques Used: Inhibition, Over Expression, Activity Assay

Image Search Results

Journal: bioRxiv

Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

doi: 10.64898/2025.12.24.696284

Figure Lengend Snippet: A) AML cell lines including both VEN-susceptible and resistant (Molm-13, Molm-13/VR, HL-60, HL-60/VR, U937), and AML PDX cells (2016-1, 2016-7) were treated with different concentrations of CX-4945 and VEN alone or in combination with indicated doses for 48 h. Cell viability was assessed using WST reagent and cell viability was calculated relative to vehicle-treated cells as 100%. B) ZIP synergy scores for CX-4945 and VEN combination in different AML cell lines and PDX cells were shown. ZIP scores greater than 10 indicates ‘synergy’, and 0-10 indicate ‘additive’ activity between CX-4945 and VEN. C-D) AML cells (Molm-13, Molm-13/VR, PDX 2016-7) were treated with CX-4945 and VEN alone or in combination for 24 h and stained with Annexin V/7AAD for analyzing apoptosis by flow cytometry ( C ). Relative apoptosis was calculated by normalizing to vehicle treated cells ( D ). The data are presented as mean ± SD (n=2-4). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 by one-way ANOVA (Holm-Sidak’s multiple comparisons test) denotes statistical significance. E) AML cell lines (Molm-13, Molm-13/VR) were treated with CX-4945 and VEN alone or in combination for 24 h and the surface expression of chemoresistance markers (CD47 and CD123) was analyzed by flow cytometry. F) Schematic showing the workflow for dynamic BH3 profiling to measure drug-induced priming of BH3 peptides in AML cells. The difference in Cyt c release (%) with and without drug treatment was presented as delta priming. Created with BioRender.com . G) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides with and without CX-4945 treatment and calculated the delta priming. The data are presented as mean ± SEM (n=2) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test).

Article Snippet: CX-4945 (#HY-50855B) and venetoclax (#HY-15531) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Activity Assay, Staining, Flow Cytometry, Expressing

Journal: bioRxiv

Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

doi: 10.64898/2025.12.24.696284

Figure Lengend Snippet: A) The common mechanisms that govern cellular MCL-1 levels at transcription, translation, and post-translation levels are depicted. The signaling cascade mediated through CK2, PI3K/AKT, and mTOR regulate transcription and translation of MCL-1 isoforms (L-large, S-short, ES-extra short). MCL-1L (anti-apoptotic) undergoes caspase-mediated cleavage to form pro-apoptotic shorter MCL-1 isoforms (S & ES) that can induce cellular apoptosis independent of BAX and BAK. Created using BioRender.com . B) The levels of MCL-1 isoforms (L and ES) were measured by immunoblotting in AML cell lines and PDX cells after 24h of treatment with CX-4945 and VEN alone or in combination. C) Quantification of MCL-1 transcript levels after treatment with CX-4945 and VEN alone or in combination for 24h in indicated AML cell lines and PDX cells by qRT-PCR. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. D) Immunoblotting analysis of AML cell lines (Molm-13, Molm-13/VR, U937) and PDX (2016-1, 2016-7) cells after 24h of treatment with CX-4945 and VEN alone or in combination. β-Actin was used as a loading control. Representative blots from two to three independent experiments were shown.

Article Snippet: CX-4945 (#HY-50855B) and venetoclax (#HY-15531) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Western Blot, Quantitative RT-PCR, Control

Journal: bioRxiv

Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

doi: 10.64898/2025.12.24.696284

Figure Lengend Snippet: A) Schematic depicting the treatment plan in AML patient-derived xenograft (PDX) mouse model. Similar scheme followed for cell line-derived xenograft (CDX) mice except the analysis after two-weeks of treatment. The NRG-S mice were irradiated and intravenously injected with AML cell lines Molm-13VR (0.25×10 6 cells/mouse), U937 (1×10 4 cells/mouse), and PDX 2016-7 (0.5×10 6 cells/mouse) and randomized into experimental groups (Vehicle, CX-4945, VEN, and CX+VEN Como). The drug treatment started after one week of cell transplantation and followed up for survival analysis or analysis after two-weeks of treatment (only for PDX). B-F) After two weeks of drug treatment, mice injected with PDX 2016-7 cells were sacrificed and spleen weight was recorded ( B ). The cells collected from spleens were analyzed by flow cytometry to analyze percent hCD45 positive cells ( C ). D-F) CBC analysis was performed on PDX 2016-7 mice after two-weeks of drug treatment by Hemavet analyzer. The data for B-F are presented as mean ± SD (n=7-8) and analyzed by one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 indicates statistical significance, while ‘ns’ denotes ‘not significant’. G) Immunoblotting analysis of spleen cells collected from PDX 2016-7 mice after two-weeks of treatment with CX-4945, VEN, and CX+VEN combo. The data for three different experimental animals was presented. H-J) Kaplan-Meyer survival analysis of 2016-7 PDX ( H ), Molm-13/VR CDX ( I ), and U937 CDX ( J ) mice after treatment with CX-4945, VEN and CX+VEN combo. The overall median survival (MS) days for each experimental group of PDX and CDX mice were provided next to the legend. *p<0.05, **p<0.01 and ***p<0.001 by Gehan-Breslow-Wilcoxon test indicates statistical significance.

Article Snippet: CX-4945 (#HY-50855B) and venetoclax (#HY-15531) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Derivative Assay, Irradiation, Injection, Transplantation Assay, Flow Cytometry, Western Blot

Journal: bioRxiv

Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

doi: 10.64898/2025.12.24.696284

Figure Lengend Snippet: A) AML cells from patients were surfaced stained with different fluorescent labeled antibodies and analyzed for the expression of markers for LSCs (CD34, CD38, TIM3) and chemoresistance (CD47 and CD123) by flow cytometry. B) The basal level expression of CK2α, BCL-XL, and CK2 activity (p-CK2 substrate) was measured in primary AML cells by immunoblotting analysis. C) The basal level apoptosis and viability of primary AML patient cells was assessed after 12-24h of post-thaw using Annexin V & dead cell kit for Muse cell analyzer. The patient cells with high basal level apoptosis were omitted and the ones used for further testing were highlighted using red square box. D & E) AML patient cells were treated with CX-4945 and VEN alone and in combination for 24 h and surface stained for different cell surface markers along with annexin V. The relative apoptosis in bulk cells ( D ), LSCs (CD34+CD38−) and chemoresistant (CD47+CD123-) subpopulations were calculated by normalizing the percent apoptosis in vehicle treated cells ( E ). The data are presented as mean ± SEM (n=6-7) and analyzed via one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, and ***p<0.001 considered as statistically significant.

Article Snippet: CX-4945 (#HY-50855B) and venetoclax (#HY-15531) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Staining, Labeling, Expressing, Flow Cytometry, Activity Assay, Western Blot

Journal: bioRxiv

Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

doi: 10.64898/2025.12.24.696284

Figure Lengend Snippet: Inhibition of CK2-mediated signaling through CX-4945 negatively affect cell survival pathways (PI3K/AKT/mTOR, NF-κB pathways) and anti-apoptotic proteins (MCL-1L and BCL-XL). Downregulation of anti-apoptotic BCL2 members (MCL-1L, BCL-XL) further enhance BCL-2 dependency and enhance VEN-mediated apoptosis in VR-AML cells. Overexpression of pro-apoptotic MCL-1ES isoform that can mediate mitochondrial depolarization independent of BAX/BAK contribute to potentiate VEN activity. Moreover, the transcriptome of VR-AML cells followed by CX-4945 and VEN combination treatment showed reversal of molecular gene signatures associated with VEN resistance and result in potentiated apoptosis in VR-AML cells. The signaling targeted by CX-4945 and VEN are represented by dotted lines. Created using BioRender.com .

Article Snippet: CX-4945 (#HY-50855B) and venetoclax (#HY-15531) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Inhibition, Over Expression, Activity Assay

CK2 is overexpressed in T-ALL compared to normal mononuclear cells . ( A ) Schematic showing PIK3CD and PIKFYVE genes in the PI3K pathway. ( B ) Baseline protein levels of CK2α, pCK2, and IKAROS in the T cell leukemia cell panel (CCRF-CEM, MOLT4, and primary T-ALL cells (labeled T-ALL#1)) were measured by Western blot and compared to peripheral blood mononuclear cells (MNCs). The protein level is graphed relative to vinculin as a loading control. ( C ) Radio-immunoblot showing phospho-IKAROS in a leukemia cell panel (CCRF-CEM, MOLT4, and primary T-ALL cells (labeled ALL#1-5)) compared to MNCs. ( D ) Radio-immunoblot showing a decrease in the phospho-IKAROS level following CX-4945 treatment. MOLT4 cells were treated with 10 μM of CX-4945 for 24 h. EV, endosomal vesicle; PIK3CD, phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit delta; and PIKFYVE, phosphoinositide kinase, FYVE-type zinc finger containing; PI3K, phosphoinositide 3-kinase; P, phospho; PIP2, phosphatidylinositol 4,5-bisphosphate; PIP3, phosphatidylinositol 3,4,5-trisphosphate; PDK1, phosphoinositide-dependent kinase; PI3P, phosphatidylinositol-3-phosphate; PI(3,5)P2, phosphotydile inositol 3,5-biphosphate.

Journal: International Journal of Molecular Sciences

Article Title: Transcriptional Regulation of PIK3CD and PIKFYVE in T-Cell Acute Lymphoblastic Leukemia by IKAROS and Protein Kinase CK2

doi: 10.3390/ijms22020819

Figure Lengend Snippet: CK2 is overexpressed in T-ALL compared to normal mononuclear cells . ( A ) Schematic showing PIK3CD and PIKFYVE genes in the PI3K pathway. ( B ) Baseline protein levels of CK2α, pCK2, and IKAROS in the T cell leukemia cell panel (CCRF-CEM, MOLT4, and primary T-ALL cells (labeled T-ALL#1)) were measured by Western blot and compared to peripheral blood mononuclear cells (MNCs). The protein level is graphed relative to vinculin as a loading control. ( C ) Radio-immunoblot showing phospho-IKAROS in a leukemia cell panel (CCRF-CEM, MOLT4, and primary T-ALL cells (labeled ALL#1-5)) compared to MNCs. ( D ) Radio-immunoblot showing a decrease in the phospho-IKAROS level following CX-4945 treatment. MOLT4 cells were treated with 10 μM of CX-4945 for 24 h. EV, endosomal vesicle; PIK3CD, phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit delta; and PIKFYVE, phosphoinositide kinase, FYVE-type zinc finger containing; PI3K, phosphoinositide 3-kinase; P, phospho; PIP2, phosphatidylinositol 4,5-bisphosphate; PIP3, phosphatidylinositol 3,4,5-trisphosphate; PDK1, phosphoinositide-dependent kinase; PI3P, phosphatidylinositol-3-phosphate; PI(3,5)P2, phosphotydile inositol 3,5-biphosphate.

Article Snippet: CK2 inhibitor CX-4945 sodium salt was purchased from MedChem Express (Monmouth Junction, NJ, USA).

Techniques: Labeling, Western Blot, Control

CK2 inhibition restores IKAROS DNA binding and repression of PIK3CD and PIKFYVE . MOLT4, CEM, and T-ALL#1 cells were treated with 10 μM of CX-4945 for 24 h. IKAROS binding to the ( A ) PIK3CD and ( B ) PIKFYVE promoter region was confirmed using qChIP assay in vehicle- and CX-4945-treated cells. Results are mean ± SD of triplicates representative of one of three independent experiments. Molecular inhibition of CK2α in CEM and MOLT4 cells was achieved using shRNA. Two of four shRNAs showed a significant and similar decrease in CK2α. qRT-PCR shows the mRNA level of ( C ) CK2α and ( D ) PIK3CD and PIKFYVE in CK2-silenced MOLT4 (left panel) and CEM (right panel) cells. CEM and MOLT4 cells were treated with 10 and 20 μM of CX-4945 for 48 h, and T-ALL#1 primary leukemia cells were treated with 10 μM of CX-4945 for 12 h. mRNA and protein were extracted. ( E ) The mRNA level of PIK3CD and PIKFYVE was measured in CX-4945-treated CEM, MOLT4, and T-ALL#1 cells. ( F ) AKT and phosphorylated-AKT (p-AKT) protein levels were measured by Western blot. The protein level is expressed relative to vinculin. The p -value summaries are as follows: p ≤ 0.05 (*); p < 0.01 (**).

Journal: International Journal of Molecular Sciences

Article Title: Transcriptional Regulation of PIK3CD and PIKFYVE in T-Cell Acute Lymphoblastic Leukemia by IKAROS and Protein Kinase CK2

doi: 10.3390/ijms22020819

Figure Lengend Snippet: CK2 inhibition restores IKAROS DNA binding and repression of PIK3CD and PIKFYVE . MOLT4, CEM, and T-ALL#1 cells were treated with 10 μM of CX-4945 for 24 h. IKAROS binding to the ( A ) PIK3CD and ( B ) PIKFYVE promoter region was confirmed using qChIP assay in vehicle- and CX-4945-treated cells. Results are mean ± SD of triplicates representative of one of three independent experiments. Molecular inhibition of CK2α in CEM and MOLT4 cells was achieved using shRNA. Two of four shRNAs showed a significant and similar decrease in CK2α. qRT-PCR shows the mRNA level of ( C ) CK2α and ( D ) PIK3CD and PIKFYVE in CK2-silenced MOLT4 (left panel) and CEM (right panel) cells. CEM and MOLT4 cells were treated with 10 and 20 μM of CX-4945 for 48 h, and T-ALL#1 primary leukemia cells were treated with 10 μM of CX-4945 for 12 h. mRNA and protein were extracted. ( E ) The mRNA level of PIK3CD and PIKFYVE was measured in CX-4945-treated CEM, MOLT4, and T-ALL#1 cells. ( F ) AKT and phosphorylated-AKT (p-AKT) protein levels were measured by Western blot. The protein level is expressed relative to vinculin. The p -value summaries are as follows: p ≤ 0.05 (*); p < 0.01 (**).

Article Snippet: CK2 inhibitor CX-4945 sodium salt was purchased from MedChem Express (Monmouth Junction, NJ, USA).

Techniques: Inhibition, Binding Assay, shRNA, Quantitative RT-PCR, Western Blot

Model illustration of regulation of PI3K pathway genes PIK3CD and PIKFYVE in T-ALL by CK2 and IKAROS.

Journal: International Journal of Molecular Sciences

Article Title: Transcriptional Regulation of PIK3CD and PIKFYVE in T-Cell Acute Lymphoblastic Leukemia by IKAROS and Protein Kinase CK2

doi: 10.3390/ijms22020819

Figure Lengend Snippet: Model illustration of regulation of PI3K pathway genes PIK3CD and PIKFYVE in T-ALL by CK2 and IKAROS.

Article Snippet: CK2 inhibitor CX-4945 sodium salt was purchased from MedChem Express (Monmouth Junction, NJ, USA).

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