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Fig. 2 PF-477736 selectively kills <t>LIMD1−/−cells</t> independent of Chk1 inhibition. A Dose–response curve of SCH900776 in HeLa isogenic LIMD1−/−lines. Cells were treated for 4 days before measuring viability and calculating surviving fraction (n = 3). B Bar chart of SF50 values from panel (A) (n = 3, one-way ANOVA). C Surviving fraction of HeLa isogenic LIMD1−/−lines transfected with siRNA against CHEK1 at 50 nM and 20 nM for 72 h (n = 3, two-way ANOVA). ns p > 0.05. D Immunoblot of Chk1 and LIMD1 in HeLa isogenic LIMD1−/−lines transfected with siRNA against CHEK1 (20 nM, 72 h) (n = 3).
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Fig. 2 PF-477736 selectively kills LIMD1−/−cells independent of Chk1 inhibition. A Dose–response curve of SCH900776 in HeLa isogenic LIMD1−/−lines. Cells were treated for 4 days before measuring viability and calculating surviving fraction (n = 3). B Bar chart of SF50 values from panel (A) (n = 3, one-way ANOVA). C Surviving fraction of HeLa isogenic LIMD1−/−lines transfected with siRNA against CHEK1 at 50 nM and 20 nM for 72 h (n = 3, two-way ANOVA). ns p > 0.05. D Immunoblot of Chk1 and LIMD1 in HeLa isogenic LIMD1−/−lines transfected with siRNA against CHEK1 (20 nM, 72 h) (n = 3).

Journal: Cell death & disease

Article Title: Targeted therapy for LIMD1-deficient non-small cell lung cancer subtypes.

doi: 10.1038/s41419-021-04355-7

Figure Lengend Snippet: Fig. 2 PF-477736 selectively kills LIMD1−/−cells independent of Chk1 inhibition. A Dose–response curve of SCH900776 in HeLa isogenic LIMD1−/−lines. Cells were treated for 4 days before measuring viability and calculating surviving fraction (n = 3). B Bar chart of SF50 values from panel (A) (n = 3, one-way ANOVA). C Surviving fraction of HeLa isogenic LIMD1−/−lines transfected with siRNA against CHEK1 at 50 nM and 20 nM for 72 h (n = 3, two-way ANOVA). ns p > 0.05. D Immunoblot of Chk1 and LIMD1 in HeLa isogenic LIMD1−/−lines transfected with siRNA against CHEK1 (20 nM, 72 h) (n = 3).

Article Snippet: Lysates were electrophoresed on acrylamide gels of appropriate acrylamide percentage, transferred onto PVDF membranes and immunoblotted using the following antibodies: LIMD1 (in house), β-actin (Sigma #A1978), Total PARP (CST #9532), Cleaved PARP (CST #6704), Caspase 7 (CST #12827), Caspase 9 (CST #9508), Caspase 3 (CST #9668) and Cleaved Caspase 9 (CST #7237), Chk1 (CST #2360).

Techniques: Inhibition, Transfection, Western Blot

Fig. 3 PF-477736 is a broad-spectrum kinase inhibitor that elicits LIMD1−/−-specific cellular changes in the phosphoproteome. A Heatmap showing remaining kinase activity of a panel of in vitro kinases upon 3 µM PF4-77736 treatment in DiscoverX KINOMEscan assay. B Venn diagram representing the proportion and number of kinases inhibited to less than 35%, 10% and 1% of control activity. C Waterfall plot of kinases most inhibited by PF-477736 (3 µM) in the in vitro kinase assay. D Volcano plot of phosphosite changes between 1 µM PF- 477736-treated and DMSO control lysates in isogenic HeLa lines. Cells were harvested following 1 h drug treatment. No significant phosphosite changes were induced by PF-477736 in the LIMD1+/+ cell line, compared with 54 reduced and 119 increased phosphosites in the LIMD1−/−cell line. Cut-off point for statistically significant phosphosite is a false discovery rate of >0.05 and S0 of 0.01 (n = 3). E Kinase substrate enrichment analysis (KSEA) of phosphoproteomics shows kinases significantly affected by PF-477736 treatment in LIMD1+/+ (grey) or LIMD1−/−cells (green) *p ≤0.05, **p ≤0.01, ***p ≤0.001.

Journal: Cell death & disease

Article Title: Targeted therapy for LIMD1-deficient non-small cell lung cancer subtypes.

doi: 10.1038/s41419-021-04355-7

Figure Lengend Snippet: Fig. 3 PF-477736 is a broad-spectrum kinase inhibitor that elicits LIMD1−/−-specific cellular changes in the phosphoproteome. A Heatmap showing remaining kinase activity of a panel of in vitro kinases upon 3 µM PF4-77736 treatment in DiscoverX KINOMEscan assay. B Venn diagram representing the proportion and number of kinases inhibited to less than 35%, 10% and 1% of control activity. C Waterfall plot of kinases most inhibited by PF-477736 (3 µM) in the in vitro kinase assay. D Volcano plot of phosphosite changes between 1 µM PF- 477736-treated and DMSO control lysates in isogenic HeLa lines. Cells were harvested following 1 h drug treatment. No significant phosphosite changes were induced by PF-477736 in the LIMD1+/+ cell line, compared with 54 reduced and 119 increased phosphosites in the LIMD1−/−cell line. Cut-off point for statistically significant phosphosite is a false discovery rate of >0.05 and S0 of 0.01 (n = 3). E Kinase substrate enrichment analysis (KSEA) of phosphoproteomics shows kinases significantly affected by PF-477736 treatment in LIMD1+/+ (grey) or LIMD1−/−cells (green) *p ≤0.05, **p ≤0.01, ***p ≤0.001.

Article Snippet: Lysates were electrophoresed on acrylamide gels of appropriate acrylamide percentage, transferred onto PVDF membranes and immunoblotted using the following antibodies: LIMD1 (in house), β-actin (Sigma #A1978), Total PARP (CST #9532), Cleaved PARP (CST #6704), Caspase 7 (CST #12827), Caspase 9 (CST #9508), Caspase 3 (CST #9668) and Cleaved Caspase 9 (CST #7237), Chk1 (CST #2360).

Techniques: Activity Assay, In Vitro, Control, Kinase Assay, Phospho-proteomics

Fig. 4 PF-477736 treatment is proof-of-concept inhibitor of LIMD1-deficient lung cancers. A Immunoblot of isogenic LIMD1−/−small airway epithelial cells (SAEC) and control. B Dose–response of PF-477736 in isogenic LIMD1−/−SAEC. Cells were treated twice prior to measuring cell viability and calculating surviving fraction (n = 3). C Immunoblot of LIMD1 in a panel of lung adenocarcinoma cell lines (representative blot from n = 3). D Pearson’s correlation coefficient between LIMD1 protein expression and surviving fraction of indicated cell line after treatment with 1 µM PF-477736. E Relative tumour growth of subcutaneous A549 isogenic xenografts implanted into the flank of NOD/SCID mice. Mice were treated twice on indicated days with vehicle or PF-477736 (7.5 mg/kg per dose) (n = 10 per group). F, G Immunohistochemical staining and scoring of Ki67 (F) and cleaved caspase-3 (G) in mouse xenograft tumours (n = 10 per group, two-way ANOVA).

Journal: Cell death & disease

Article Title: Targeted therapy for LIMD1-deficient non-small cell lung cancer subtypes.

doi: 10.1038/s41419-021-04355-7

Figure Lengend Snippet: Fig. 4 PF-477736 treatment is proof-of-concept inhibitor of LIMD1-deficient lung cancers. A Immunoblot of isogenic LIMD1−/−small airway epithelial cells (SAEC) and control. B Dose–response of PF-477736 in isogenic LIMD1−/−SAEC. Cells were treated twice prior to measuring cell viability and calculating surviving fraction (n = 3). C Immunoblot of LIMD1 in a panel of lung adenocarcinoma cell lines (representative blot from n = 3). D Pearson’s correlation coefficient between LIMD1 protein expression and surviving fraction of indicated cell line after treatment with 1 µM PF-477736. E Relative tumour growth of subcutaneous A549 isogenic xenografts implanted into the flank of NOD/SCID mice. Mice were treated twice on indicated days with vehicle or PF-477736 (7.5 mg/kg per dose) (n = 10 per group). F, G Immunohistochemical staining and scoring of Ki67 (F) and cleaved caspase-3 (G) in mouse xenograft tumours (n = 10 per group, two-way ANOVA).

Article Snippet: Lysates were electrophoresed on acrylamide gels of appropriate acrylamide percentage, transferred onto PVDF membranes and immunoblotted using the following antibodies: LIMD1 (in house), β-actin (Sigma #A1978), Total PARP (CST #9532), Cleaved PARP (CST #6704), Caspase 7 (CST #12827), Caspase 9 (CST #9508), Caspase 3 (CST #9668) and Cleaved Caspase 9 (CST #7237), Chk1 (CST #2360).

Techniques: Western Blot, Control, Expressing, Immunohistochemical staining, Staining