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Proteintech anti recql4 antibody
<t>RECQL4</t> immunohistochemistry. Representative microphotographs of RECQL4 immunohistochemistry staining. (A) HGG with high RECQL4 expression (H-score: 180). (B) HGG with intermediate RECQL4 expression (H-score: 80). (C) Angiocentric glioma with low RECQL4 expression (H-score: 10). HGG, adult-type diffuse high-grade glioma.
Anti Recql4 Antibody, supplied by Proteintech, 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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Proteintech recql4
<t>RECQL4</t> immunohistochemistry. Representative microphotographs of RECQL4 immunohistochemistry staining. (A) HGG with high RECQL4 expression (H-score: 180). (B) HGG with intermediate RECQL4 expression (H-score: 80). (C) Angiocentric glioma with low RECQL4 expression (H-score: 10). HGG, adult-type diffuse high-grade glioma.
Recql4, supplied by Proteintech, 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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Proteintech recql4 expression immunohistochemistry ihc
<t>RECQL4</t> immunohistochemistry. Representative microphotographs of RECQL4 immunohistochemistry staining. (A) HGG with high RECQL4 expression (H-score: 180). (B) HGG with intermediate RECQL4 expression (H-score: 80). (C) Angiocentric glioma with low RECQL4 expression (H-score: 10). HGG, adult-type diffuse high-grade glioma.
Recql4 Expression Immunohistochemistry Ihc, supplied by Proteintech, 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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Santa Cruz Biotechnology recql4 gene
Fig. 1 | Association of MTBP and <t>phospho-RecQL4</t> with pre-RCs at baseline and dormant replication origins. A Baseline and dormant origins. Top, experimental procedure. SIRT1 deficient (SIRT1Null) HCT116 cells were complemented with either WT-SIRT1 (WTSIRT1) or H363Y-SIRT1 (an inactive mutant; MutSIRT1) cDNA15. Replication origins were mapped using nascent strand sequencing (NS-seq)15. Bottom, a gen- ome browser view of NS-seq coverage across a representative genomic region on chromosome 1. Baseline origins (black rectangles) are defined as active in both WTSIRT1 and MutSIRT1 cells, whereas dormant origins (dashed black rectangles) are active only in MutSIRT1 cells. Pre-RNase treatment serves as a control, as RNA primer removal allows lambda exonuclease to digest nascent DNA, eliminating origin peaks. B Nascent strand abundance (initiation) at baseline and dormant origins in cells harboring WTSIRT1 (WT) or MutSIRT1 (Mut). C HCT116 cells containing auxin – inducible degron MCM2 (MCM2-mAID) were complemented with either intact (WT) or S139A substituted MCM215. IAA (auxin, 500 μM for 16 h) depleted the endogenous MCM2-mAID. Complementation with MCM2-S139A, but not WT MCM2, inhibited replication initiation15 (Supplementary Fig. 1E). D The abundance of pMCM2-S139, MCM2, Treslin, MTBP and pRecQL4-S89 in whole cell (WCE) and
Recql4 Gene, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology crispr cas9 kit
Fig. 1 | Association of MTBP and <t>phospho-RecQL4</t> with pre-RCs at baseline and dormant replication origins. A Baseline and dormant origins. Top, experimental procedure. SIRT1 deficient (SIRT1Null) HCT116 cells were complemented with either WT-SIRT1 (WTSIRT1) or H363Y-SIRT1 (an inactive mutant; MutSIRT1) cDNA15. Replication origins were mapped using nascent strand sequencing (NS-seq)15. Bottom, a gen- ome browser view of NS-seq coverage across a representative genomic region on chromosome 1. Baseline origins (black rectangles) are defined as active in both WTSIRT1 and MutSIRT1 cells, whereas dormant origins (dashed black rectangles) are active only in MutSIRT1 cells. Pre-RNase treatment serves as a control, as RNA primer removal allows lambda exonuclease to digest nascent DNA, eliminating origin peaks. B Nascent strand abundance (initiation) at baseline and dormant origins in cells harboring WTSIRT1 (WT) or MutSIRT1 (Mut). C HCT116 cells containing auxin – inducible degron MCM2 (MCM2-mAID) were complemented with either intact (WT) or S139A substituted MCM215. IAA (auxin, 500 μM for 16 h) depleted the endogenous MCM2-mAID. Complementation with MCM2-S139A, but not WT MCM2, inhibited replication initiation15 (Supplementary Fig. 1E). D The abundance of pMCM2-S139, MCM2, Treslin, MTBP and pRecQL4-S89 in whole cell (WCE) and
Crispr Cas9 Kit, supplied by Santa Cruz Biotechnology, 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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Image Search Results


RECQL4 immunohistochemistry. Representative microphotographs of RECQL4 immunohistochemistry staining. (A) HGG with high RECQL4 expression (H-score: 180). (B) HGG with intermediate RECQL4 expression (H-score: 80). (C) Angiocentric glioma with low RECQL4 expression (H-score: 10). HGG, adult-type diffuse high-grade glioma.

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 immunohistochemistry. Representative microphotographs of RECQL4 immunohistochemistry staining. (A) HGG with high RECQL4 expression (H-score: 180). (B) HGG with intermediate RECQL4 expression (H-score: 80). (C) Angiocentric glioma with low RECQL4 expression (H-score: 10). HGG, adult-type diffuse high-grade glioma.

Article Snippet: Immunohistochemistry (IHC) with anti-RECQL4 antibody (Proteintech 17008-1-AP, 1:50) was utilized on a tissue microarray (TMA) consisting of 21 low-grade gliomas ([LGG]; 17 low-grade circumscribed gliomas [LGCG] and 4 low-grade diffuse gliomas [LGDG] all of which were angiocentric gliomas, AG); 41 adult-type diffuse high-grade gliomas ([HGG], grade 4); and 99 nerve sheath tumors, comprising 67 neurofibromas and 32 malignant peripheral nerve sheath tumors (MPNST).

Techniques: Immunohistochemistry, Staining, Expressing

RECQL4 immunohistochemistry in gliomas. (A) RECQL4 immunohistochemical H-scores in low-grade circumscribed glioma (LGCG, n = 42), low-grade diffuse glioma (LGDG, n = 4), and high-grade glioma (HGG, n = 65); expression differed significantly across the groups (Kruskal–Wallis test, χ 2 = 8.78, df = 2, P = 0.012). (B) RECQL4 immunohistochemical H-scores in low-grade circumscribed glioma subtypes, namely subependymal giant-cell astrocytoma (SEGA, n = 2), pilocytic astrocytoma (PA, n = 7), and pleomorphic xanthoastrocytoma (PXA, n = 8). H-scores were similar across groups (Kruskal–Wallis test, χ 2 = 0.003, df = 2, P = 0.999).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 immunohistochemistry in gliomas. (A) RECQL4 immunohistochemical H-scores in low-grade circumscribed glioma (LGCG, n = 42), low-grade diffuse glioma (LGDG, n = 4), and high-grade glioma (HGG, n = 65); expression differed significantly across the groups (Kruskal–Wallis test, χ 2 = 8.78, df = 2, P = 0.012). (B) RECQL4 immunohistochemical H-scores in low-grade circumscribed glioma subtypes, namely subependymal giant-cell astrocytoma (SEGA, n = 2), pilocytic astrocytoma (PA, n = 7), and pleomorphic xanthoastrocytoma (PXA, n = 8). H-scores were similar across groups (Kruskal–Wallis test, χ 2 = 0.003, df = 2, P = 0.999).

Article Snippet: Immunohistochemistry (IHC) with anti-RECQL4 antibody (Proteintech 17008-1-AP, 1:50) was utilized on a tissue microarray (TMA) consisting of 21 low-grade gliomas ([LGG]; 17 low-grade circumscribed gliomas [LGCG] and 4 low-grade diffuse gliomas [LGDG] all of which were angiocentric gliomas, AG); 41 adult-type diffuse high-grade gliomas ([HGG], grade 4); and 99 nerve sheath tumors, comprising 67 neurofibromas and 32 malignant peripheral nerve sheath tumors (MPNST).

Techniques: Immunohistochemistry, Immunohistochemical staining, Expressing

RECQL4 immunohistochemistry in nerve sheath tumors. RECQL4 H-scores across cases of neurofibromas ( n = 67), NF1-related malignant peripheral nerve sheath tumors (MPNST, n = 24), and sporadic MPNST ( n = 8). Global comparison performed using Kruskal–Wallis test (χ² = 20.54, df = 2, P = 0.000035).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 immunohistochemistry in nerve sheath tumors. RECQL4 H-scores across cases of neurofibromas ( n = 67), NF1-related malignant peripheral nerve sheath tumors (MPNST, n = 24), and sporadic MPNST ( n = 8). Global comparison performed using Kruskal–Wallis test (χ² = 20.54, df = 2, P = 0.000035).

Article Snippet: Immunohistochemistry (IHC) with anti-RECQL4 antibody (Proteintech 17008-1-AP, 1:50) was utilized on a tissue microarray (TMA) consisting of 21 low-grade gliomas ([LGG]; 17 low-grade circumscribed gliomas [LGCG] and 4 low-grade diffuse gliomas [LGDG] all of which were angiocentric gliomas, AG); 41 adult-type diffuse high-grade gliomas ([HGG], grade 4); and 99 nerve sheath tumors, comprising 67 neurofibromas and 32 malignant peripheral nerve sheath tumors (MPNST).

Techniques: Immunohistochemistry, Comparison

RECQL4 knockdown in glioma. Glioma cell line U251 with its RECQL4-knockdowns (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 knockdown in glioma. Glioma cell line U251 with its RECQL4-knockdowns (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Article Snippet: Immunohistochemistry (IHC) with anti-RECQL4 antibody (Proteintech 17008-1-AP, 1:50) was utilized on a tissue microarray (TMA) consisting of 21 low-grade gliomas ([LGG]; 17 low-grade circumscribed gliomas [LGCG] and 4 low-grade diffuse gliomas [LGDG] all of which were angiocentric gliomas, AG); 41 adult-type diffuse high-grade gliomas ([HGG], grade 4); and 99 nerve sheath tumors, comprising 67 neurofibromas and 32 malignant peripheral nerve sheath tumors (MPNST).

Techniques: Knockdown, Plasmid Preparation, Control

RECQL4 knockdown in MPNST. Malignant peripheral nerve sheath tumor cell line NF90-8 with its RECQL4-knockdowns (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 knockdown in MPNST. Malignant peripheral nerve sheath tumor cell line NF90-8 with its RECQL4-knockdowns (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Article Snippet: Immunohistochemistry (IHC) with anti-RECQL4 antibody (Proteintech 17008-1-AP, 1:50) was utilized on a tissue microarray (TMA) consisting of 21 low-grade gliomas ([LGG]; 17 low-grade circumscribed gliomas [LGCG] and 4 low-grade diffuse gliomas [LGDG] all of which were angiocentric gliomas, AG); 41 adult-type diffuse high-grade gliomas ([HGG], grade 4); and 99 nerve sheath tumors, comprising 67 neurofibromas and 32 malignant peripheral nerve sheath tumors (MPNST).

Techniques: Knockdown, Plasmid Preparation, Control

RECQL4 knockdown in MPNST. Malignant peripheral nerve sheath tumor cell line ST88-14 with its RECQL4-knockouts (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 knockdown in MPNST. Malignant peripheral nerve sheath tumor cell line ST88-14 with its RECQL4-knockouts (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Article Snippet: Immunohistochemistry (IHC) with anti-RECQL4 antibody (Proteintech 17008-1-AP, 1:50) was utilized on a tissue microarray (TMA) consisting of 21 low-grade gliomas ([LGG]; 17 low-grade circumscribed gliomas [LGCG] and 4 low-grade diffuse gliomas [LGDG] all of which were angiocentric gliomas, AG); 41 adult-type diffuse high-grade gliomas ([HGG], grade 4); and 99 nerve sheath tumors, comprising 67 neurofibromas and 32 malignant peripheral nerve sheath tumors (MPNST).

Techniques: Knockdown, Plasmid Preparation, Control

ATR inhibition decreases cell growth in tumor cells with RECQL4 loss. Effect of ATR kinase inhibition on cell proliferation of glioma and malignant peripheral nerve sheath tumor (MPNST) cell lines and their RECQL4-knockouts. Glioma U251 cell line survival fraction at different dosages of AZD6738 (Upper left) and VE-821 (Upper right). MPNST NF90-8 cell line survival fraction at different dosages of AZD6738 (Mid left)) and VE-821 (Mid right). MPNST ST88-14 cell line survival fraction at different dosages of AZD6738 (Lower left) and VE-821 (Lower right)).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: ATR inhibition decreases cell growth in tumor cells with RECQL4 loss. Effect of ATR kinase inhibition on cell proliferation of glioma and malignant peripheral nerve sheath tumor (MPNST) cell lines and their RECQL4-knockouts. Glioma U251 cell line survival fraction at different dosages of AZD6738 (Upper left) and VE-821 (Upper right). MPNST NF90-8 cell line survival fraction at different dosages of AZD6738 (Mid left)) and VE-821 (Mid right). MPNST ST88-14 cell line survival fraction at different dosages of AZD6738 (Lower left) and VE-821 (Lower right)).

Article Snippet: Immunohistochemistry (IHC) with anti-RECQL4 antibody (Proteintech 17008-1-AP, 1:50) was utilized on a tissue microarray (TMA) consisting of 21 low-grade gliomas ([LGG]; 17 low-grade circumscribed gliomas [LGCG] and 4 low-grade diffuse gliomas [LGDG] all of which were angiocentric gliomas, AG); 41 adult-type diffuse high-grade gliomas ([HGG], grade 4); and 99 nerve sheath tumors, comprising 67 neurofibromas and 32 malignant peripheral nerve sheath tumors (MPNST).

Techniques: Inhibition

RECQL4 immunohistochemistry. Representative microphotographs of RECQL4 immunohistochemistry staining. (A) HGG with high RECQL4 expression (H-score: 180). (B) HGG with intermediate RECQL4 expression (H-score: 80). (C) Angiocentric glioma with low RECQL4 expression (H-score: 10). HGG, adult-type diffuse high-grade glioma.

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 immunohistochemistry. Representative microphotographs of RECQL4 immunohistochemistry staining. (A) HGG with high RECQL4 expression (H-score: 180). (B) HGG with intermediate RECQL4 expression (H-score: 80). (C) Angiocentric glioma with low RECQL4 expression (H-score: 10). HGG, adult-type diffuse high-grade glioma.

Article Snippet: The primary antibody utilized for Western blot analysis was RECQL4 (17008-1-AP, 1:2000, Proteintech, Rosemont, IL, USA), the secondary antibodies used was anti-rabbit IgG HRP-linked (#7074, 1:5000, Cell Signaling Technology).

Techniques: Immunohistochemistry, Staining, Expressing

RECQL4 immunohistochemistry in gliomas. (A) RECQL4 immunohistochemical H-scores in low-grade circumscribed glioma (LGCG, n = 42), low-grade diffuse glioma (LGDG, n = 4), and high-grade glioma (HGG, n = 65); expression differed significantly across the groups (Kruskal–Wallis test, χ 2 = 8.78, df = 2, P = 0.012). (B) RECQL4 immunohistochemical H-scores in low-grade circumscribed glioma subtypes, namely subependymal giant-cell astrocytoma (SEGA, n = 2), pilocytic astrocytoma (PA, n = 7), and pleomorphic xanthoastrocytoma (PXA, n = 8). H-scores were similar across groups (Kruskal–Wallis test, χ 2 = 0.003, df = 2, P = 0.999).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 immunohistochemistry in gliomas. (A) RECQL4 immunohistochemical H-scores in low-grade circumscribed glioma (LGCG, n = 42), low-grade diffuse glioma (LGDG, n = 4), and high-grade glioma (HGG, n = 65); expression differed significantly across the groups (Kruskal–Wallis test, χ 2 = 8.78, df = 2, P = 0.012). (B) RECQL4 immunohistochemical H-scores in low-grade circumscribed glioma subtypes, namely subependymal giant-cell astrocytoma (SEGA, n = 2), pilocytic astrocytoma (PA, n = 7), and pleomorphic xanthoastrocytoma (PXA, n = 8). H-scores were similar across groups (Kruskal–Wallis test, χ 2 = 0.003, df = 2, P = 0.999).

Article Snippet: The primary antibody utilized for Western blot analysis was RECQL4 (17008-1-AP, 1:2000, Proteintech, Rosemont, IL, USA), the secondary antibodies used was anti-rabbit IgG HRP-linked (#7074, 1:5000, Cell Signaling Technology).

Techniques: Immunohistochemistry, Immunohistochemical staining, Expressing

RECQL4 immunohistochemistry in nerve sheath tumors. RECQL4 H-scores across cases of neurofibromas ( n = 67), NF1-related malignant peripheral nerve sheath tumors (MPNST, n = 24), and sporadic MPNST ( n = 8). Global comparison performed using Kruskal–Wallis test (χ² = 20.54, df = 2, P = 0.000035).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 immunohistochemistry in nerve sheath tumors. RECQL4 H-scores across cases of neurofibromas ( n = 67), NF1-related malignant peripheral nerve sheath tumors (MPNST, n = 24), and sporadic MPNST ( n = 8). Global comparison performed using Kruskal–Wallis test (χ² = 20.54, df = 2, P = 0.000035).

Article Snippet: The primary antibody utilized for Western blot analysis was RECQL4 (17008-1-AP, 1:2000, Proteintech, Rosemont, IL, USA), the secondary antibodies used was anti-rabbit IgG HRP-linked (#7074, 1:5000, Cell Signaling Technology).

Techniques: Immunohistochemistry, Comparison

RECQL4 knockdown in glioma. Glioma cell line U251 with its RECQL4-knockdowns (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 knockdown in glioma. Glioma cell line U251 with its RECQL4-knockdowns (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Article Snippet: The primary antibody utilized for Western blot analysis was RECQL4 (17008-1-AP, 1:2000, Proteintech, Rosemont, IL, USA), the secondary antibodies used was anti-rabbit IgG HRP-linked (#7074, 1:5000, Cell Signaling Technology).

Techniques: Knockdown, Plasmid Preparation, Control

RECQL4 knockdown in MPNST. Malignant peripheral nerve sheath tumor cell line NF90-8 with its RECQL4-knockdowns (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 knockdown in MPNST. Malignant peripheral nerve sheath tumor cell line NF90-8 with its RECQL4-knockdowns (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Article Snippet: The primary antibody utilized for Western blot analysis was RECQL4 (17008-1-AP, 1:2000, Proteintech, Rosemont, IL, USA), the secondary antibodies used was anti-rabbit IgG HRP-linked (#7074, 1:5000, Cell Signaling Technology).

Techniques: Knockdown, Plasmid Preparation, Control

RECQL4 knockdown in MPNST. Malignant peripheral nerve sheath tumor cell line ST88-14 with its RECQL4-knockouts (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: RECQL4 knockdown in MPNST. Malignant peripheral nerve sheath tumor cell line ST88-14 with its RECQL4-knockouts (RECQL4sh2 and RECQL4sh5) and empty vector control (pLKO.1). Cell numbers measured at multiple time points (upper). Percentage of BrdU-positive cells (lower left). Percentage of apoptotic cells (lower right).

Article Snippet: The primary antibody utilized for Western blot analysis was RECQL4 (17008-1-AP, 1:2000, Proteintech, Rosemont, IL, USA), the secondary antibodies used was anti-rabbit IgG HRP-linked (#7074, 1:5000, Cell Signaling Technology).

Techniques: Knockdown, Plasmid Preparation, Control

ATR inhibition decreases cell growth in tumor cells with RECQL4 loss. Effect of ATR kinase inhibition on cell proliferation of glioma and malignant peripheral nerve sheath tumor (MPNST) cell lines and their RECQL4-knockouts. Glioma U251 cell line survival fraction at different dosages of AZD6738 (Upper left) and VE-821 (Upper right). MPNST NF90-8 cell line survival fraction at different dosages of AZD6738 (Mid left)) and VE-821 (Mid right). MPNST ST88-14 cell line survival fraction at different dosages of AZD6738 (Lower left) and VE-821 (Lower right)).

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications

doi: 10.1093/jnen/nlaf129

Figure Lengend Snippet: ATR inhibition decreases cell growth in tumor cells with RECQL4 loss. Effect of ATR kinase inhibition on cell proliferation of glioma and malignant peripheral nerve sheath tumor (MPNST) cell lines and their RECQL4-knockouts. Glioma U251 cell line survival fraction at different dosages of AZD6738 (Upper left) and VE-821 (Upper right). MPNST NF90-8 cell line survival fraction at different dosages of AZD6738 (Mid left)) and VE-821 (Mid right). MPNST ST88-14 cell line survival fraction at different dosages of AZD6738 (Lower left) and VE-821 (Lower right)).

Article Snippet: The primary antibody utilized for Western blot analysis was RECQL4 (17008-1-AP, 1:2000, Proteintech, Rosemont, IL, USA), the secondary antibodies used was anti-rabbit IgG HRP-linked (#7074, 1:5000, Cell Signaling Technology).

Techniques: Inhibition

Fig. 1 | Association of MTBP and phospho-RecQL4 with pre-RCs at baseline and dormant replication origins. A Baseline and dormant origins. Top, experimental procedure. SIRT1 deficient (SIRT1Null) HCT116 cells were complemented with either WT-SIRT1 (WTSIRT1) or H363Y-SIRT1 (an inactive mutant; MutSIRT1) cDNA15. Replication origins were mapped using nascent strand sequencing (NS-seq)15. Bottom, a gen- ome browser view of NS-seq coverage across a representative genomic region on chromosome 1. Baseline origins (black rectangles) are defined as active in both WTSIRT1 and MutSIRT1 cells, whereas dormant origins (dashed black rectangles) are active only in MutSIRT1 cells. Pre-RNase treatment serves as a control, as RNA primer removal allows lambda exonuclease to digest nascent DNA, eliminating origin peaks. B Nascent strand abundance (initiation) at baseline and dormant origins in cells harboring WTSIRT1 (WT) or MutSIRT1 (Mut). C HCT116 cells containing auxin – inducible degron MCM2 (MCM2-mAID) were complemented with either intact (WT) or S139A substituted MCM215. IAA (auxin, 500 μM for 16 h) depleted the endogenous MCM2-mAID. Complementation with MCM2-S139A, but not WT MCM2, inhibited replication initiation15 (Supplementary Fig. 1E). D The abundance of pMCM2-S139, MCM2, Treslin, MTBP and pRecQL4-S89 in whole cell (WCE) and

Journal: Nature communications

Article Title: Selective interactions at pre-replication complexes categorize baseline and dormant origins.

doi: 10.1038/s41467-025-59509-4

Figure Lengend Snippet: Fig. 1 | Association of MTBP and phospho-RecQL4 with pre-RCs at baseline and dormant replication origins. A Baseline and dormant origins. Top, experimental procedure. SIRT1 deficient (SIRT1Null) HCT116 cells were complemented with either WT-SIRT1 (WTSIRT1) or H363Y-SIRT1 (an inactive mutant; MutSIRT1) cDNA15. Replication origins were mapped using nascent strand sequencing (NS-seq)15. Bottom, a gen- ome browser view of NS-seq coverage across a representative genomic region on chromosome 1. Baseline origins (black rectangles) are defined as active in both WTSIRT1 and MutSIRT1 cells, whereas dormant origins (dashed black rectangles) are active only in MutSIRT1 cells. Pre-RNase treatment serves as a control, as RNA primer removal allows lambda exonuclease to digest nascent DNA, eliminating origin peaks. B Nascent strand abundance (initiation) at baseline and dormant origins in cells harboring WTSIRT1 (WT) or MutSIRT1 (Mut). C HCT116 cells containing auxin – inducible degron MCM2 (MCM2-mAID) were complemented with either intact (WT) or S139A substituted MCM215. IAA (auxin, 500 μM for 16 h) depleted the endogenous MCM2-mAID. Complementation with MCM2-S139A, but not WT MCM2, inhibited replication initiation15 (Supplementary Fig. 1E). D The abundance of pMCM2-S139, MCM2, Treslin, MTBP and pRecQL4-S89 in whole cell (WCE) and

Article Snippet: The RecQL4 gene was depleted from HCT116 cells using a CRISPR-Cas9 kit (Santa Cruz, cat # sc-403224), and clones were confirmed using western blotting for RecQL4.

Techniques: Mutagenesis, Sequencing, Control