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Structured Review

Proteintech krt1
A Schematic of the RNA pull down experiment for the identification of proteins associated with lncPSMB1 . B Silver staining of lncPSMB1 pulldown in HEPM cells. C List of the top ten differentially expressed proteins identified by mass spectrometry, FDR < 0.01. D Relative RNA levels of lncPSMB1 detected by RT-qPCR after RIP for <t>KRT1,</t> KRT9 and KRT10 in HEPM cells. E , F HEPM cells with either negative control, lncPSMB1 overexpression, or lncPSMB1 knockdown were exposed to cycloheximide (CHX, 100 μg/mL) for indicated time intervals. KRT1 protein abundance was subsequently detected by western blot. G HEPM cells were treated with 10 μg/ml MG132 before harvesting. KRT1 was immunoprecipitated using a KRT1-specific antibody, and ubiquitinated forms were subsequently detected via immunoblotting with anti-Ubi antibody. H The apoptosis rate was detected in HEPM cells after siRNA-mediated silencing of KRT1 . I Cell proliferation was assessed by using the CCK-8 in HEPM cells after siRNA-mediated silencing of KRT1 . J Relative RNA levels of lncPSMB1 cell-apoptosis target genes in HEPM cells after siRNA-mediated silencing of KRT1 . K Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing a decrease in cell apoptosis. L Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing an increase in cell proliferation. * p < 0.05, ** p < 0.01, *** p < 0.001. ns not significant.
Krt1, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 47 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/krt1/Cytokeratin+1-specific+Antibody/pmc12307944-289-0-7
Average 95 stars, based on 47 article reviews
krt1 - by Bioz Stars, 2026-09
95/100 stars

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1) Product Images from "Genetic modulation of lncPSMB1 confers non-syndromic cleft lip with or without cleft palate susceptibility by promoting cell apoptosis"

Article Title: Genetic modulation of lncPSMB1 confers non-syndromic cleft lip with or without cleft palate susceptibility by promoting cell apoptosis

Journal: Communications Biology

doi: 10.1038/s42003-025-08563-1

A Schematic of the RNA pull down experiment for the identification of proteins associated with lncPSMB1 . B Silver staining of lncPSMB1 pulldown in HEPM cells. C List of the top ten differentially expressed proteins identified by mass spectrometry, FDR < 0.01. D Relative RNA levels of lncPSMB1 detected by RT-qPCR after RIP for KRT1, KRT9 and KRT10 in HEPM cells. E , F HEPM cells with either negative control, lncPSMB1 overexpression, or lncPSMB1 knockdown were exposed to cycloheximide (CHX, 100 μg/mL) for indicated time intervals. KRT1 protein abundance was subsequently detected by western blot. G HEPM cells were treated with 10 μg/ml MG132 before harvesting. KRT1 was immunoprecipitated using a KRT1-specific antibody, and ubiquitinated forms were subsequently detected via immunoblotting with anti-Ubi antibody. H The apoptosis rate was detected in HEPM cells after siRNA-mediated silencing of KRT1 . I Cell proliferation was assessed by using the CCK-8 in HEPM cells after siRNA-mediated silencing of KRT1 . J Relative RNA levels of lncPSMB1 cell-apoptosis target genes in HEPM cells after siRNA-mediated silencing of KRT1 . K Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing a decrease in cell apoptosis. L Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing an increase in cell proliferation. * p < 0.05, ** p < 0.01, *** p < 0.001. ns not significant.
Figure Legend Snippet: A Schematic of the RNA pull down experiment for the identification of proteins associated with lncPSMB1 . B Silver staining of lncPSMB1 pulldown in HEPM cells. C List of the top ten differentially expressed proteins identified by mass spectrometry, FDR < 0.01. D Relative RNA levels of lncPSMB1 detected by RT-qPCR after RIP for KRT1, KRT9 and KRT10 in HEPM cells. E , F HEPM cells with either negative control, lncPSMB1 overexpression, or lncPSMB1 knockdown were exposed to cycloheximide (CHX, 100 μg/mL) for indicated time intervals. KRT1 protein abundance was subsequently detected by western blot. G HEPM cells were treated with 10 μg/ml MG132 before harvesting. KRT1 was immunoprecipitated using a KRT1-specific antibody, and ubiquitinated forms were subsequently detected via immunoblotting with anti-Ubi antibody. H The apoptosis rate was detected in HEPM cells after siRNA-mediated silencing of KRT1 . I Cell proliferation was assessed by using the CCK-8 in HEPM cells after siRNA-mediated silencing of KRT1 . J Relative RNA levels of lncPSMB1 cell-apoptosis target genes in HEPM cells after siRNA-mediated silencing of KRT1 . K Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing a decrease in cell apoptosis. L Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing an increase in cell proliferation. * p < 0.05, ** p < 0.01, *** p < 0.001. ns not significant.

Techniques Used: Silver Staining, Mass Spectrometry, Quantitative RT-PCR, Negative Control, Over Expression, Knockdown, Quantitative Proteomics, Western Blot, Immunoprecipitation, CCK-8 Assay

SNP rs4710839 altered the MYC binding affinity and regulated the expression of the lncPSMB1 . In addition, lncPSMB1 interacted with KRT1 to activate the cell apoptotic process and ultimately increased the risk of NSCL/P.
Figure Legend Snippet: SNP rs4710839 altered the MYC binding affinity and regulated the expression of the lncPSMB1 . In addition, lncPSMB1 interacted with KRT1 to activate the cell apoptotic process and ultimately increased the risk of NSCL/P.

Techniques Used: Binding Assay, Expressing



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A Schematic of the RNA pull down experiment for the identification of proteins associated with lncPSMB1 . B Silver staining of lncPSMB1 pulldown in HEPM cells. C List of the top ten differentially expressed proteins identified by mass spectrometry, FDR < 0.01. D Relative RNA levels of lncPSMB1 detected by RT-qPCR after RIP for <t>KRT1,</t> KRT9 and KRT10 in HEPM cells. E , F HEPM cells with either negative control, lncPSMB1 overexpression, or lncPSMB1 knockdown were exposed to cycloheximide (CHX, 100 μg/mL) for indicated time intervals. KRT1 protein abundance was subsequently detected by western blot. G HEPM cells were treated with 10 μg/ml MG132 before harvesting. KRT1 was immunoprecipitated using a KRT1-specific antibody, and ubiquitinated forms were subsequently detected via immunoblotting with anti-Ubi antibody. H The apoptosis rate was detected in HEPM cells after siRNA-mediated silencing of KRT1 . I Cell proliferation was assessed by using the CCK-8 in HEPM cells after siRNA-mediated silencing of KRT1 . J Relative RNA levels of lncPSMB1 cell-apoptosis target genes in HEPM cells after siRNA-mediated silencing of KRT1 . K Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing a decrease in cell apoptosis. L Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing an increase in cell proliferation. * p < 0.05, ** p < 0.01, *** p < 0.001. ns not significant.
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A Schematic of the RNA pull down experiment for the identification of proteins associated with lncPSMB1 . B Silver staining of lncPSMB1 pulldown in HEPM cells. C List of the top ten differentially expressed proteins identified by mass spectrometry, FDR < 0.01. D Relative RNA levels of lncPSMB1 detected by RT-qPCR after RIP for <t>KRT1,</t> KRT9 and KRT10 in HEPM cells. E , F HEPM cells with either negative control, lncPSMB1 overexpression, or lncPSMB1 knockdown were exposed to cycloheximide (CHX, 100 μg/mL) for indicated time intervals. KRT1 protein abundance was subsequently detected by western blot. G HEPM cells were treated with 10 μg/ml MG132 before harvesting. KRT1 was immunoprecipitated using a KRT1-specific antibody, and <t>ubiquitinated</t> forms were subsequently detected via immunoblotting with anti-Ubi antibody. H The apoptosis rate was detected in HEPM cells after siRNA-mediated silencing of KRT1 . I Cell proliferation was assessed by using the CCK-8 in HEPM cells after siRNA-mediated silencing of KRT1 . J Relative RNA levels of lncPSMB1 cell-apoptosis target genes in HEPM cells after siRNA-mediated silencing of KRT1 . K Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing a decrease in cell apoptosis. L Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing an increase in cell proliferation. * p < 0.05, ** p < 0.01, *** p < 0.001. ns not significant.
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A Schematic of the RNA pull down experiment for the identification of proteins associated with lncPSMB1 . B Silver staining of lncPSMB1 pulldown in HEPM cells. C List of the top ten differentially expressed proteins identified by mass spectrometry, FDR < 0.01. D Relative RNA levels of lncPSMB1 detected by RT-qPCR after RIP for <t>KRT1,</t> KRT9 and KRT10 in HEPM cells. E , F HEPM cells with either negative control, lncPSMB1 overexpression, or lncPSMB1 knockdown were exposed to cycloheximide (CHX, 100 μg/mL) for indicated time intervals. KRT1 protein abundance was subsequently detected by western blot. G HEPM cells were treated with 10 μg/ml MG132 before harvesting. KRT1 was immunoprecipitated using a KRT1-specific antibody, and <t>ubiquitinated</t> forms were subsequently detected via immunoblotting with anti-Ubi antibody. H The apoptosis rate was detected in HEPM cells after siRNA-mediated silencing of KRT1 . I Cell proliferation was assessed by using the CCK-8 in HEPM cells after siRNA-mediated silencing of KRT1 . J Relative RNA levels of lncPSMB1 cell-apoptosis target genes in HEPM cells after siRNA-mediated silencing of KRT1 . K Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing a decrease in cell apoptosis. L Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing an increase in cell proliferation. * p < 0.05, ** p < 0.01, *** p < 0.001. ns not significant.
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Image Search Results


The effect of RELA, MIRI, and EPL on mRNA expression of keratinocyte differentiation markers. Mice were treated, skin samples collected and RNA isolated for RT-qPCR as in . ( A ) Ivl expression was significantly upregulated in MIRI-treated mice compared with those receiving VEH or RELA. ( B ) Krt10 expression was significantly upregulated in MIRI-treated mice compared with treatment with VEH and EPL. ( C ) Lor expression was significantly upregulated in MIRI-treated mice compared with VEH control. ( D ) Krt1 mRNA expression was not significantly altered by RELA, MIRI or EPL. n = 7–8; * p ≤ 0.05 and ** p ≤ 0.01 as indicated.

Journal: International Journal of Molecular Sciences

Article Title: The Effect of Glucocorticoid and Mineralocorticoid Receptor Antagonists in the Skin of Aged Female Mice

doi: 10.3390/ijms26178346

Figure Lengend Snippet: The effect of RELA, MIRI, and EPL on mRNA expression of keratinocyte differentiation markers. Mice were treated, skin samples collected and RNA isolated for RT-qPCR as in . ( A ) Ivl expression was significantly upregulated in MIRI-treated mice compared with those receiving VEH or RELA. ( B ) Krt10 expression was significantly upregulated in MIRI-treated mice compared with treatment with VEH and EPL. ( C ) Lor expression was significantly upregulated in MIRI-treated mice compared with VEH control. ( D ) Krt1 mRNA expression was not significantly altered by RELA, MIRI or EPL. n = 7–8; * p ≤ 0.05 and ** p ≤ 0.01 as indicated.

Article Snippet: Krt1 , ThermoFisher Scientific , Mm00492992_g1.

Techniques: Expressing, Isolation, Quantitative RT-PCR, Control

A Schematic of the RNA pull down experiment for the identification of proteins associated with lncPSMB1 . B Silver staining of lncPSMB1 pulldown in HEPM cells. C List of the top ten differentially expressed proteins identified by mass spectrometry, FDR < 0.01. D Relative RNA levels of lncPSMB1 detected by RT-qPCR after RIP for KRT1, KRT9 and KRT10 in HEPM cells. E , F HEPM cells with either negative control, lncPSMB1 overexpression, or lncPSMB1 knockdown were exposed to cycloheximide (CHX, 100 μg/mL) for indicated time intervals. KRT1 protein abundance was subsequently detected by western blot. G HEPM cells were treated with 10 μg/ml MG132 before harvesting. KRT1 was immunoprecipitated using a KRT1-specific antibody, and ubiquitinated forms were subsequently detected via immunoblotting with anti-Ubi antibody. H The apoptosis rate was detected in HEPM cells after siRNA-mediated silencing of KRT1 . I Cell proliferation was assessed by using the CCK-8 in HEPM cells after siRNA-mediated silencing of KRT1 . J Relative RNA levels of lncPSMB1 cell-apoptosis target genes in HEPM cells after siRNA-mediated silencing of KRT1 . K Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing a decrease in cell apoptosis. L Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing an increase in cell proliferation. * p < 0.05, ** p < 0.01, *** p < 0.001. ns not significant.

Journal: Communications Biology

Article Title: Genetic modulation of lncPSMB1 confers non-syndromic cleft lip with or without cleft palate susceptibility by promoting cell apoptosis

doi: 10.1038/s42003-025-08563-1

Figure Lengend Snippet: A Schematic of the RNA pull down experiment for the identification of proteins associated with lncPSMB1 . B Silver staining of lncPSMB1 pulldown in HEPM cells. C List of the top ten differentially expressed proteins identified by mass spectrometry, FDR < 0.01. D Relative RNA levels of lncPSMB1 detected by RT-qPCR after RIP for KRT1, KRT9 and KRT10 in HEPM cells. E , F HEPM cells with either negative control, lncPSMB1 overexpression, or lncPSMB1 knockdown were exposed to cycloheximide (CHX, 100 μg/mL) for indicated time intervals. KRT1 protein abundance was subsequently detected by western blot. G HEPM cells were treated with 10 μg/ml MG132 before harvesting. KRT1 was immunoprecipitated using a KRT1-specific antibody, and ubiquitinated forms were subsequently detected via immunoblotting with anti-Ubi antibody. H The apoptosis rate was detected in HEPM cells after siRNA-mediated silencing of KRT1 . I Cell proliferation was assessed by using the CCK-8 in HEPM cells after siRNA-mediated silencing of KRT1 . J Relative RNA levels of lncPSMB1 cell-apoptosis target genes in HEPM cells after siRNA-mediated silencing of KRT1 . K Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing a decrease in cell apoptosis. L Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing an increase in cell proliferation. * p < 0.05, ** p < 0.01, *** p < 0.001. ns not significant.

Article Snippet: KRT1 and KRT10 antibodies were derived from Proteintech (Cat# 16848-1-AP for KRT1, Cat# 18343-1-AP for KRT10).

Techniques: Silver Staining, Mass Spectrometry, Quantitative RT-PCR, Negative Control, Over Expression, Knockdown, Quantitative Proteomics, Western Blot, Immunoprecipitation, CCK-8 Assay

SNP rs4710839 altered the MYC binding affinity and regulated the expression of the lncPSMB1 . In addition, lncPSMB1 interacted with KRT1 to activate the cell apoptotic process and ultimately increased the risk of NSCL/P.

Journal: Communications Biology

Article Title: Genetic modulation of lncPSMB1 confers non-syndromic cleft lip with or without cleft palate susceptibility by promoting cell apoptosis

doi: 10.1038/s42003-025-08563-1

Figure Lengend Snippet: SNP rs4710839 altered the MYC binding affinity and regulated the expression of the lncPSMB1 . In addition, lncPSMB1 interacted with KRT1 to activate the cell apoptotic process and ultimately increased the risk of NSCL/P.

Article Snippet: KRT1 and KRT10 antibodies were derived from Proteintech (Cat# 16848-1-AP for KRT1, Cat# 18343-1-AP for KRT10).

Techniques: Binding Assay, Expressing

A Schematic of the RNA pull down experiment for the identification of proteins associated with lncPSMB1 . B Silver staining of lncPSMB1 pulldown in HEPM cells. C List of the top ten differentially expressed proteins identified by mass spectrometry, FDR < 0.01. D Relative RNA levels of lncPSMB1 detected by RT-qPCR after RIP for KRT1, KRT9 and KRT10 in HEPM cells. E , F HEPM cells with either negative control, lncPSMB1 overexpression, or lncPSMB1 knockdown were exposed to cycloheximide (CHX, 100 μg/mL) for indicated time intervals. KRT1 protein abundance was subsequently detected by western blot. G HEPM cells were treated with 10 μg/ml MG132 before harvesting. KRT1 was immunoprecipitated using a KRT1-specific antibody, and ubiquitinated forms were subsequently detected via immunoblotting with anti-Ubi antibody. H The apoptosis rate was detected in HEPM cells after siRNA-mediated silencing of KRT1 . I Cell proliferation was assessed by using the CCK-8 in HEPM cells after siRNA-mediated silencing of KRT1 . J Relative RNA levels of lncPSMB1 cell-apoptosis target genes in HEPM cells after siRNA-mediated silencing of KRT1 . K Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing a decrease in cell apoptosis. L Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing an increase in cell proliferation. * p < 0.05, ** p < 0.01, *** p < 0.001. ns not significant.

Journal: Communications Biology

Article Title: Genetic modulation of lncPSMB1 confers non-syndromic cleft lip with or without cleft palate susceptibility by promoting cell apoptosis

doi: 10.1038/s42003-025-08563-1

Figure Lengend Snippet: A Schematic of the RNA pull down experiment for the identification of proteins associated with lncPSMB1 . B Silver staining of lncPSMB1 pulldown in HEPM cells. C List of the top ten differentially expressed proteins identified by mass spectrometry, FDR < 0.01. D Relative RNA levels of lncPSMB1 detected by RT-qPCR after RIP for KRT1, KRT9 and KRT10 in HEPM cells. E , F HEPM cells with either negative control, lncPSMB1 overexpression, or lncPSMB1 knockdown were exposed to cycloheximide (CHX, 100 μg/mL) for indicated time intervals. KRT1 protein abundance was subsequently detected by western blot. G HEPM cells were treated with 10 μg/ml MG132 before harvesting. KRT1 was immunoprecipitated using a KRT1-specific antibody, and ubiquitinated forms were subsequently detected via immunoblotting with anti-Ubi antibody. H The apoptosis rate was detected in HEPM cells after siRNA-mediated silencing of KRT1 . I Cell proliferation was assessed by using the CCK-8 in HEPM cells after siRNA-mediated silencing of KRT1 . J Relative RNA levels of lncPSMB1 cell-apoptosis target genes in HEPM cells after siRNA-mediated silencing of KRT1 . K Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing a decrease in cell apoptosis. L Knockdown of KRT1 rescued lncPSMB1 overexpression phenotype by inducing an increase in cell proliferation. * p < 0.05, ** p < 0.01, *** p < 0.001. ns not significant.

Article Snippet: The immunoprecipitates were analyzed by Western blotting, and the abundance of ubiquitinated KRT1 was detected by an anti-ubiquitin antibody (Cat# 10201-2-AP, Proteintech).

Techniques: Silver Staining, Mass Spectrometry, Quantitative RT-PCR, Negative Control, Over Expression, Knockdown, Quantitative Proteomics, Western Blot, Immunoprecipitation, CCK-8 Assay

SNP rs4710839 altered the MYC binding affinity and regulated the expression of the lncPSMB1 . In addition, lncPSMB1 interacted with KRT1 to activate the cell apoptotic process and ultimately increased the risk of NSCL/P.

Journal: Communications Biology

Article Title: Genetic modulation of lncPSMB1 confers non-syndromic cleft lip with or without cleft palate susceptibility by promoting cell apoptosis

doi: 10.1038/s42003-025-08563-1

Figure Lengend Snippet: SNP rs4710839 altered the MYC binding affinity and regulated the expression of the lncPSMB1 . In addition, lncPSMB1 interacted with KRT1 to activate the cell apoptotic process and ultimately increased the risk of NSCL/P.

Article Snippet: The immunoprecipitates were analyzed by Western blotting, and the abundance of ubiquitinated KRT1 was detected by an anti-ubiquitin antibody (Cat# 10201-2-AP, Proteintech).

Techniques: Binding Assay, Expressing