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cortical pcs 400 011 (ATCC)

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ATCC cortical pcs 400 011
Cortical Pcs 400 011, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 57 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pcs+400+011/Primary+Renal+Cortical+Epithelial+Cells%3B+Normal%2C+Human/bio_rxiv__64898__2026__04__23__720088-28-2-2
Average 94 stars, based on 57 article reviews

cortical pcs 400 011 - by Bioz Stars, 2026-09

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Article Title: Treating cognitive decline and other neurodegenerative conditions by selectively removing senescent cells from neurological tissue
Article Snippet: Cell strains included Primary Renal Cortical Cells, ATCC Cat # PCS-400-011 (FIG. 20), HCA2 foreskin fibroblast cells (FIG. 21), Primary Small Airway Epithelial Cells, ATCC Cat # PCS-301-010 (lung) (FIG. 22), human pooled Preadipocyte from patients (Pread) (FIG. 23), Mouse embryonic fibroblast extracted from C57Bl6 mice (MEF) (FIG. 24), Primary Coronary Artery Smooth Muscle, ATCC Cat # PCS-100-021 (Smth Mscl) (FIG. 25).

Article Title: Treating cardiovascular disease by selectively eliminating senescent cells
Article Snippet: Cell strains included Primary Renal Cortical Cells, ATCC Cat # PCS-400-011 (FIG. 20), HCA2 foreskin fibroblast cells (FIG. 21), Primary Small Airway Epithelial Cells, ATCC Cat # PCS-301-010 (lung) (FIG. 22), human pooled Preadipocyte from patients (Pread) (FIG. 23), Mouse embryonic fibroblast extracted from C571316 mice (MEF) (FIG. 24), Primary Coronary Artery Smooth Muscle, ATCC Cat # PCS-100-021 (Smth Mscl) (FIG. 25).

Article Title: Unit dose of an aryl sulfonamide that is effective for treating eye disease and averting potential vision loss
Article Snippet: Cell strains included Primary Renal Cortical Cells, ATCC Cat# PCS-400-011 (FIG. 20), HCA2 foreskin fibroblast cells (FIG. 21), Primary Small Airway Epithelial Cells, ATCC Cat#PCS-301-010 (lung) (FIG. 22), human pooled Preadipocyte from patients (Pread) (FIG. 23), Mouse embryonic fibroblast extracted from C57B16 mice (MEF) (FIG. 24), Primary Coronary Artery Smooth Muscle, ATCC Cat# PCS-100-021 (Smth Mscl) (FIG. 25).

Article Title: Treating pulmonary conditions by selectively removing senescent cells from the lung using an intermittent dosing regimen
Article Snippet: Cell strains included Primary Renal Cortical Cells, ATCC Cat# PCS-400-011 (FIG. 20), HCA2 foreskin fibroblast cells (FIG. 21), Primary Small Airway Epithelial Cells, ATCC Cat# PCS-301-010 (lung) (FIG. 22), human pooled Preadipocyte from patients (Pread) (FIG. 23), Mouse embryonic fibroblast extracted from C57Bl6 mice (MEF) (FIG. 24), Primary Coronary Artery Smooth Muscle, ATCC Cat# PCS-100-021 (Smth Mscl) (FIG. 25).

Article Title: Methods and compositions for killing senescent cells and for treating senescence-associated diseases and disorders using an inhibitor of Akt kinase
Article Snippet: Cell strains included Primary Renal Cortical Cells, ATCC Cat# PCS-400-011 (FIG. 20), HCA2 foreskin fibroblast cells (FIG. 21), Primary Small Airway Epithelial Cells, ATCC Cat# PCS-301-010 (lung) (FIG. 22), human pooled Preadipocyte from patients (Pread) (FIG. 23), Mouse embryonic fibroblast extracted from C571316 mice (MEF) (FIG. 24), Primary Coronary Artery Smooth Muscle, ATCC Cat# PCS-100-021 (Smth Mscl) (FIG. 25).

Article Title: Removing senescent cells from a mixed cell population or tissue using a phosphoinositide 3-kinase (PI3K) inhibitor
Article Snippet: Cell strains included Primary Renal Cortical Cells, ATCC Cat# PCS-400-011 (FIG. 20), HCA2 foreskin fibroblast cells (FIG. 21), Primary Small Airway Epithelial Cells, ATCC Cat# PCS-301-010 (lung) (FIG. 22), human pooled Preadipocyte from patients (Pread) (FIG. 23), Mouse embryonic fibroblast extracted from C57BI6 mice (MEF) (FIG. 24), Primary Coronary Artery Smooth Muscle, ATCC Cat# PCS-100-021 (Smth Mscl) (FIG. 25).

Article Title: Use of sulfonamide inhibitors of BCL-2 and BCL-xL to treat ophthalmic disease by selectively removing senescent cells
Article Snippet: Cell strains included Primary Renal Cortical Cells, ATCC Cat# PCS-400-011 (FIG. 20), HCA2 foreskin fibroblast cells (FIG. 21), Primary Small Airway Epithelial Cells, ATCC Cat# PCS-301-010 (lung) (FIG. 22), human pooled Preadipocyte from patients (Pread) (FIG. 23), Mouse embryonic fibroblast extracted from C57Bl6 mice (MEF) (FIG. 24), Primary Coronary Artery Smooth Muscle, ATCC Cat# PCS-100-021 (Smth Mscl) (FIG. 25).

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cortical pcs 400 011 (ATCC)

ATCC cortical pcs 400 011
Cortical Pcs 400 011, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pcs+400+011/Primary+Renal+Cortical+Epithelial+Cells%3B+Normal%2C+Human/bio_rxiv__64898__2026__04__23__720088-28-2-2
Average 94 stars, based on 1 article reviews

cortical pcs 400 011 - by Bioz Stars, 2026-09

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human renal epithelial cells (ATCC)

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$Transcriptional heterogeneity and lineage‐resolved progression in primary senescence at single‐cell level. (A) Experimental overview. Renal <t>epithelial</t> cells were irradiated (IR; 10 Gy, 10 days) to induce primary senescence, with quiescent controls (QUI; 0.01% serum, 3 days) processed for scRNA‐seq. (B) Expression levels of senescence and SASP‐related genes in senescent relative to the controls (QUI, n = 3; IR, n = 3). (C) Secreted IL‐6 levels in CM measured using ELISA (QUI, n = 6; IR, n = 6). Data are presented as the means ± the standard error of the mean (unpaired two‐tailed t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001). (D) UMAP of primary dataset showing clusters grouped into non‐senescent (C4 and C9), intermediate (C0, C1, C3, and C7), and fully senescent states (C5, C6, and C8) (left). Each bar represents either IR or QUI, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of IR and QUI cells across each cluster (right). (E) Feature plots showing expression levels of proliferation and senescence‐associated genes. (F) Heatmap of pathway activity across clusters scored via gene set variation analysis, with Z ‐score normalization. (G) UMAP trajectory analysis using Slingshot identifying three senescence progression lineages. Trajectory lines overlaid on UMAP. Cell clusters are colored by pseudotime progression. (H, I) Boxplots of normalized pathway scores for DNA repair (H) and SASP‐related gene sets (I) across clusters (Kruskal–Wallis test, with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways of non‐senescent, intermediate, and fully senescent states in the primary SnCs. p‐values were calculated using a hypergeometric distribution. (K) TradeSeq‐based heatmap of temporally regulated top 500 genes along the pseudotime trajectory for lineage 3 ( p < 0.05), with representative late‐pseudotime genes highlighted.$
Human Renal Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pcs+400+011/Primary+Renal+Cortical+Epithelial+Cells%3B+Normal%2C+Human/pmc13182272-181-0-4
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renal epithelial cell line (ATCC)

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$Transcriptional heterogeneity and lineage‐resolved progression in primary senescence at single‐cell level. (A) Experimental overview. Renal <t>epithelial</t> cells were irradiated (IR; 10 Gy, 10 days) to induce primary senescence, with quiescent controls (QUI; 0.01% serum, 3 days) processed for scRNA‐seq. (B) Expression levels of senescence and SASP‐related genes in senescent relative to the controls (QUI, n = 3; IR, n = 3). (C) Secreted IL‐6 levels in CM measured using ELISA (QUI, n = 6; IR, n = 6). Data are presented as the means ± the standard error of the mean (unpaired two‐tailed t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001). (D) UMAP of primary dataset showing clusters grouped into non‐senescent (C4 and C9), intermediate (C0, C1, C3, and C7), and fully senescent states (C5, C6, and C8) (left). Each bar represents either IR or QUI, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of IR and QUI cells across each cluster (right). (E) Feature plots showing expression levels of proliferation and senescence‐associated genes. (F) Heatmap of pathway activity across clusters scored via gene set variation analysis, with Z ‐score normalization. (G) UMAP trajectory analysis using Slingshot identifying three senescence progression lineages. Trajectory lines overlaid on UMAP. Cell clusters are colored by pseudotime progression. (H, I) Boxplots of normalized pathway scores for DNA repair (H) and SASP‐related gene sets (I) across clusters (Kruskal–Wallis test, with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways of non‐senescent, intermediate, and fully senescent states in the primary SnCs. p‐values were calculated using a hypergeometric distribution. (K) TradeSeq‐based heatmap of temporally regulated top 500 genes along the pseudotime trajectory for lineage 3 ( p < 0.05), with representative late‐pseudotime genes highlighted.$
Renal Epithelial Cell Line, supplied by ATCC, 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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renal epithelial cell line - by Bioz Stars, 2026-09

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human renal cell carcinoma cell line (ATCC)

ATCC human renal cell carcinoma cell line
$Transcriptional heterogeneity and lineage‐resolved progression in primary senescence at single‐cell level. (A) Experimental overview. Renal <t>epithelial</t> cells were irradiated (IR; 10 Gy, 10 days) to induce primary senescence, with quiescent controls (QUI; 0.01% serum, 3 days) processed for scRNA‐seq. (B) Expression levels of senescence and SASP‐related genes in senescent relative to the controls (QUI, n = 3; IR, n = 3). (C) Secreted IL‐6 levels in CM measured using ELISA (QUI, n = 6; IR, n = 6). Data are presented as the means ± the standard error of the mean (unpaired two‐tailed t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001). (D) UMAP of primary dataset showing clusters grouped into non‐senescent (C4 and C9), intermediate (C0, C1, C3, and C7), and fully senescent states (C5, C6, and C8) (left). Each bar represents either IR or QUI, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of IR and QUI cells across each cluster (right). (E) Feature plots showing expression levels of proliferation and senescence‐associated genes. (F) Heatmap of pathway activity across clusters scored via gene set variation analysis, with Z ‐score normalization. (G) UMAP trajectory analysis using Slingshot identifying three senescence progression lineages. Trajectory lines overlaid on UMAP. Cell clusters are colored by pseudotime progression. (H, I) Boxplots of normalized pathway scores for DNA repair (H) and SASP‐related gene sets (I) across clusters (Kruskal–Wallis test, with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways of non‐senescent, intermediate, and fully senescent states in the primary SnCs. p‐values were calculated using a hypergeometric distribution. (K) TradeSeq‐based heatmap of temporally regulated top 500 genes along the pseudotime trajectory for lineage 3 ( p < 0.05), with representative late‐pseudotime genes highlighted.$
Human Renal Cell Carcinoma Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pcs+400+011/Primary+Renal+Cortical+Epithelial+Cells%3B+Normal%2C+Human/pmc12094832-90-25-37
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human renal cell carcinoma cell line - by Bioz Stars, 2026-09

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renal cortical tubular epithelium rcte cells (ATCC)

ATCC renal cortical tubular epithelium rcte cells
$Transcriptional heterogeneity and lineage‐resolved progression in primary senescence at single‐cell level. (A) Experimental overview. Renal <t>epithelial</t> cells were irradiated (IR; 10 Gy, 10 days) to induce primary senescence, with quiescent controls (QUI; 0.01% serum, 3 days) processed for scRNA‐seq. (B) Expression levels of senescence and SASP‐related genes in senescent relative to the controls (QUI, n = 3; IR, n = 3). (C) Secreted IL‐6 levels in CM measured using ELISA (QUI, n = 6; IR, n = 6). Data are presented as the means ± the standard error of the mean (unpaired two‐tailed t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001). (D) UMAP of primary dataset showing clusters grouped into non‐senescent (C4 and C9), intermediate (C0, C1, C3, and C7), and fully senescent states (C5, C6, and C8) (left). Each bar represents either IR or QUI, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of IR and QUI cells across each cluster (right). (E) Feature plots showing expression levels of proliferation and senescence‐associated genes. (F) Heatmap of pathway activity across clusters scored via gene set variation analysis, with Z ‐score normalization. (G) UMAP trajectory analysis using Slingshot identifying three senescence progression lineages. Trajectory lines overlaid on UMAP. Cell clusters are colored by pseudotime progression. (H, I) Boxplots of normalized pathway scores for DNA repair (H) and SASP‐related gene sets (I) across clusters (Kruskal–Wallis test, with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways of non‐senescent, intermediate, and fully senescent states in the primary SnCs. p‐values were calculated using a hypergeometric distribution. (K) TradeSeq‐based heatmap of temporally regulated top 500 genes along the pseudotime trajectory for lineage 3 ( p < 0.05), with representative late‐pseudotime genes highlighted.$
Renal Cortical Tubular Epithelium Rcte Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pcs+400+011/Primary+Renal+Cortical+Epithelial+Cells%3B+Normal%2C+Human/10__1096_slash_fj__202500128r-58-0-9
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primary human renal epithelial cells (ATCC)

ATCC primary human renal epithelial cells
$Transcriptional heterogeneity and lineage‐resolved progression in primary senescence at single‐cell level. (A) Experimental overview. Renal <t>epithelial</t> cells were irradiated (IR; 10 Gy, 10 days) to induce primary senescence, with quiescent controls (QUI; 0.01% serum, 3 days) processed for scRNA‐seq. (B) Expression levels of senescence and SASP‐related genes in senescent relative to the controls (QUI, n = 3; IR, n = 3). (C) Secreted IL‐6 levels in CM measured using ELISA (QUI, n = 6; IR, n = 6). Data are presented as the means ± the standard error of the mean (unpaired two‐tailed t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001). (D) UMAP of primary dataset showing clusters grouped into non‐senescent (C4 and C9), intermediate (C0, C1, C3, and C7), and fully senescent states (C5, C6, and C8) (left). Each bar represents either IR or QUI, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of IR and QUI cells across each cluster (right). (E) Feature plots showing expression levels of proliferation and senescence‐associated genes. (F) Heatmap of pathway activity across clusters scored via gene set variation analysis, with Z ‐score normalization. (G) UMAP trajectory analysis using Slingshot identifying three senescence progression lineages. Trajectory lines overlaid on UMAP. Cell clusters are colored by pseudotime progression. (H, I) Boxplots of normalized pathway scores for DNA repair (H) and SASP‐related gene sets (I) across clusters (Kruskal–Wallis test, with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways of non‐senescent, intermediate, and fully senescent states in the primary SnCs. p‐values were calculated using a hypergeometric distribution. (K) TradeSeq‐based heatmap of temporally regulated top 500 genes along the pseudotime trajectory for lineage 3 ( p < 0.05), with representative late‐pseudotime genes highlighted.$
Primary Human Renal Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pcs+400+011/Primary+Renal+Cortical+Epithelial+Cells%3B+Normal%2C+Human/pm40189139-58-23-28
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primary renal cortical epithelial cells hrce (ATCC)

ATCC primary renal cortical epithelial cells hrce
$Transcriptional heterogeneity and lineage‐resolved progression in primary senescence at single‐cell level. (A) Experimental overview. Renal <t>epithelial</t> cells were irradiated (IR; 10 Gy, 10 days) to induce primary senescence, with quiescent controls (QUI; 0.01% serum, 3 days) processed for scRNA‐seq. (B) Expression levels of senescence and SASP‐related genes in senescent relative to the controls (QUI, n = 3; IR, n = 3). (C) Secreted IL‐6 levels in CM measured using ELISA (QUI, n = 6; IR, n = 6). Data are presented as the means ± the standard error of the mean (unpaired two‐tailed t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001). (D) UMAP of primary dataset showing clusters grouped into non‐senescent (C4 and C9), intermediate (C0, C1, C3, and C7), and fully senescent states (C5, C6, and C8) (left). Each bar represents either IR or QUI, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of IR and QUI cells across each cluster (right). (E) Feature plots showing expression levels of proliferation and senescence‐associated genes. (F) Heatmap of pathway activity across clusters scored via gene set variation analysis, with Z ‐score normalization. (G) UMAP trajectory analysis using Slingshot identifying three senescence progression lineages. Trajectory lines overlaid on UMAP. Cell clusters are colored by pseudotime progression. (H, I) Boxplots of normalized pathway scores for DNA repair (H) and SASP‐related gene sets (I) across clusters (Kruskal–Wallis test, with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways of non‐senescent, intermediate, and fully senescent states in the primary SnCs. p‐values were calculated using a hypergeometric distribution. (K) TradeSeq‐based heatmap of temporally regulated top 500 genes along the pseudotime trajectory for lineage 3 ( p < 0.05), with representative late‐pseudotime genes highlighted.$
Primary Renal Cortical Epithelial Cells Hrce, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pcs+400+011/Primary+Renal+Cortical+Epithelial+Cells%3B+Normal%2C+Human/pm39939597-362-45-55
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normal human renal cortical epithelial cells (ATCC)

ATCC normal human renal cortical epithelial cells
$Transcriptional heterogeneity and lineage‐resolved progression in primary senescence at single‐cell level. (A) Experimental overview. Renal <t>epithelial</t> cells were irradiated (IR; 10 Gy, 10 days) to induce primary senescence, with quiescent controls (QUI; 0.01% serum, 3 days) processed for scRNA‐seq. (B) Expression levels of senescence and SASP‐related genes in senescent relative to the controls (QUI, n = 3; IR, n = 3). (C) Secreted IL‐6 levels in CM measured using ELISA (QUI, n = 6; IR, n = 6). Data are presented as the means ± the standard error of the mean (unpaired two‐tailed t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001). (D) UMAP of primary dataset showing clusters grouped into non‐senescent (C4 and C9), intermediate (C0, C1, C3, and C7), and fully senescent states (C5, C6, and C8) (left). Each bar represents either IR or QUI, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of IR and QUI cells across each cluster (right). (E) Feature plots showing expression levels of proliferation and senescence‐associated genes. (F) Heatmap of pathway activity across clusters scored via gene set variation analysis, with Z ‐score normalization. (G) UMAP trajectory analysis using Slingshot identifying three senescence progression lineages. Trajectory lines overlaid on UMAP. Cell clusters are colored by pseudotime progression. (H, I) Boxplots of normalized pathway scores for DNA repair (H) and SASP‐related gene sets (I) across clusters (Kruskal–Wallis test, with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways of non‐senescent, intermediate, and fully senescent states in the primary SnCs. p‐values were calculated using a hypergeometric distribution. (K) TradeSeq‐based heatmap of temporally regulated top 500 genes along the pseudotime trajectory for lineage 3 ( p < 0.05), with representative late‐pseudotime genes highlighted.$
Normal Human Renal Cortical Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pcs+400+011/Primary+Renal+Cortical+Epithelial+Cells%3B+Normal%2C+Human/pmc11821998__41467_2025_56873_MOESM4_ESM-89-9-17
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renal cortical epithelial cells hrce atcc (ATCC)

ATCC renal cortical epithelial cells hrce atcc
$Transcriptional heterogeneity and lineage‐resolved progression in primary senescence at single‐cell level. (A) Experimental overview. Renal <t>epithelial</t> cells were irradiated (IR; 10 Gy, 10 days) to induce primary senescence, with quiescent controls (QUI; 0.01% serum, 3 days) processed for scRNA‐seq. (B) Expression levels of senescence and SASP‐related genes in senescent relative to the controls (QUI, n = 3; IR, n = 3). (C) Secreted IL‐6 levels in CM measured using ELISA (QUI, n = 6; IR, n = 6). Data are presented as the means ± the standard error of the mean (unpaired two‐tailed t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001). (D) UMAP of primary dataset showing clusters grouped into non‐senescent (C4 and C9), intermediate (C0, C1, C3, and C7), and fully senescent states (C5, C6, and C8) (left). Each bar represents either IR or QUI, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of IR and QUI cells across each cluster (right). (E) Feature plots showing expression levels of proliferation and senescence‐associated genes. (F) Heatmap of pathway activity across clusters scored via gene set variation analysis, with Z ‐score normalization. (G) UMAP trajectory analysis using Slingshot identifying three senescence progression lineages. Trajectory lines overlaid on UMAP. Cell clusters are colored by pseudotime progression. (H, I) Boxplots of normalized pathway scores for DNA repair (H) and SASP‐related gene sets (I) across clusters (Kruskal–Wallis test, with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways of non‐senescent, intermediate, and fully senescent states in the primary SnCs. p‐values were calculated using a hypergeometric distribution. (K) TradeSeq‐based heatmap of temporally regulated top 500 genes along the pseudotime trajectory for lineage 3 ( p < 0.05), with representative late‐pseudotime genes highlighted.$
Renal Cortical Epithelial Cells Hrce Atcc, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pcs+400+011/Primary+Renal+Cortical+Epithelial+Cells%3B+Normal%2C+Human/pmc11821998__41467_2025_56873_MOESM4_ESM-89-2-7
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$Transcriptional heterogeneity and lineage‐resolved progression in primary senescence at single‐cell level. (A) Experimental overview. Renal epithelial cells were irradiated (IR; 10 Gy, 10 days) to induce primary senescence, with quiescent controls (QUI; 0.01% serum, 3 days) processed for scRNA‐seq. (B) Expression levels of senescence and SASP‐related genes in senescent relative to the controls (QUI, n = 3; IR, n = 3). (C) Secreted IL‐6 levels in CM measured using ELISA (QUI, n = 6; IR, n = 6). Data are presented as the means ± the standard error of the mean (unpaired two‐tailed t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001). (D) UMAP of primary dataset showing clusters grouped into non‐senescent (C4 and C9), intermediate (C0, C1, C3, and C7), and fully senescent states (C5, C6, and C8) (left). Each bar represents either IR or QUI, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of IR and QUI cells across each cluster (right). (E) Feature plots showing expression levels of proliferation and senescence‐associated genes. (F) Heatmap of pathway activity across clusters scored via gene set variation analysis, with Z ‐score normalization. (G) UMAP trajectory analysis using Slingshot identifying three senescence progression lineages. Trajectory lines overlaid on UMAP. Cell clusters are colored by pseudotime progression. (H, I) Boxplots of normalized pathway scores for DNA repair (H) and SASP‐related gene sets (I) across clusters (Kruskal–Wallis test, with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways of non‐senescent, intermediate, and fully senescent states in the primary SnCs. p‐values were calculated using a hypergeometric distribution. (K) TradeSeq‐based heatmap of temporally regulated top 500 genes along the pseudotime trajectory for lineage 3 ( p < 0.05), with representative late‐pseudotime genes highlighted.$

Journal: Aging Cell

Article Title: Transcriptional Profiling at Single‐Cell Resolution Reveals Diversity and Regulatory Networks of Primary and Secondary Senescent Cells

doi: 10.1111/acel.70540

Figure Lengend Snippet: Transcriptional heterogeneity and lineage‐resolved progression in primary senescence at single‐cell level. (A) Experimental overview. Renal epithelial cells were irradiated (IR; 10 Gy, 10 days) to induce primary senescence, with quiescent controls (QUI; 0.01% serum, 3 days) processed for scRNA‐seq. (B) Expression levels of senescence and SASP‐related genes in senescent relative to the controls (QUI, n = 3; IR, n = 3). (C) Secreted IL‐6 levels in CM measured using ELISA (QUI, n = 6; IR, n = 6). Data are presented as the means ± the standard error of the mean (unpaired two‐tailed t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001). (D) UMAP of primary dataset showing clusters grouped into non‐senescent (C4 and C9), intermediate (C0, C1, C3, and C7), and fully senescent states (C5, C6, and C8) (left). Each bar represents either IR or QUI, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of IR and QUI cells across each cluster (right). (E) Feature plots showing expression levels of proliferation and senescence‐associated genes. (F) Heatmap of pathway activity across clusters scored via gene set variation analysis, with Z ‐score normalization. (G) UMAP trajectory analysis using Slingshot identifying three senescence progression lineages. Trajectory lines overlaid on UMAP. Cell clusters are colored by pseudotime progression. (H, I) Boxplots of normalized pathway scores for DNA repair (H) and SASP‐related gene sets (I) across clusters (Kruskal–Wallis test, with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways of non‐senescent, intermediate, and fully senescent states in the primary SnCs. p‐values were calculated using a hypergeometric distribution. (K) TradeSeq‐based heatmap of temporally regulated top 500 genes along the pseudotime trajectory for lineage 3 ( p < 0.05), with representative late‐pseudotime genes highlighted.

Article Snippet: Human renal epithelial cells (ATCC; PCS‐400‐011) were cultured in Renal Epithelial Cell Basal Medium (ATCC; PCS‐400‐030) supplemented with the Renal Epithelial Cell Growth Kit (ATCC; PCS‐400‐040), which maintains the cultures at a final serum concentration of 0.5% and incubated at 37°C in 10% CO 2 and 3% O 2 .

Techniques: Single Cell, Irradiation, Expressing, Enzyme-linked Immunosorbent Assay, Two Tailed Test, Activity Assay

$SASP‐driven secondary senescence shows distinct transcriptional states. (A) Experimental overview: Proliferative renal epithelial cells were treated with CM from quiescent cells (QCMT) or primary senescent cells (SCMT) and separately processed for scRNA‐seq. (B) qPCR validation of senescence/SASP‐associated genes and expressed as fold changes in SCMT versus QCMT (QCMT, n = 4; SCMT, n = 3). Data are presented as the mean ± standard error of the mean. * p < 0.05, ** p < 0.01, *** p < 0.001 (two‐tailed unpaired t ‐test) (C) Secreted IL‐6 levels in CM measured by ELISA (QCMT, n = 12; SCMT, n = 8). (D) UMAP of secondary SnCs showing clusters grouped into non‐senescent (C2 and C6), intermediate (C0, C1, and C4), and fully senescent clusters (C3, C5, and C7) (left). Each bar represents either QCMT or SCMT, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of QCMT and SCMT cells across each cluster (right). (E) Feature plots of representative proliferation and senescence‐associated genes across clusters. (F) Heatmap of pathway activities across clusters ( Z ‐score normalized). (G) UMAP trajectory analysis using Slingshot identifies four lineages with distinct terminal clusters, including a senescence‐resistant endpoint. Trajectory lines indicate senescence progression, and clusters are colored by pseudotime. (H, I) Boxplots of DNA repair (H) and SASP‐related gene set scores (I) across clusters (Kruskal–Wallis two‐sided test with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways categorized into non‐senescent, intermediate, and fully senescent states. p‐values were calculated using a hypergeometric distribution. (K) Heatmap displaying temporally regulated the top 500 genes identified through tradeSeq along the pseudotime trajectory for lineage 4 in secondary senescence (hypergeometric distribution; p < 0.05).$

Journal: Aging Cell

Article Title: Transcriptional Profiling at Single‐Cell Resolution Reveals Diversity and Regulatory Networks of Primary and Secondary Senescent Cells

doi: 10.1111/acel.70540

Figure Lengend Snippet: SASP‐driven secondary senescence shows distinct transcriptional states. (A) Experimental overview: Proliferative renal epithelial cells were treated with CM from quiescent cells (QCMT) or primary senescent cells (SCMT) and separately processed for scRNA‐seq. (B) qPCR validation of senescence/SASP‐associated genes and expressed as fold changes in SCMT versus QCMT (QCMT, n = 4; SCMT, n = 3). Data are presented as the mean ± standard error of the mean. * p < 0.05, ** p < 0.01, *** p < 0.001 (two‐tailed unpaired t ‐test) (C) Secreted IL‐6 levels in CM measured by ELISA (QCMT, n = 12; SCMT, n = 8). (D) UMAP of secondary SnCs showing clusters grouped into non‐senescent (C2 and C6), intermediate (C0, C1, and C4), and fully senescent clusters (C3, C5, and C7) (left). Each bar represents either QCMT or SCMT, and each colored segment's height indicates the fraction of one of the three senescence states within that group (middle). Stacked bar chart showing the proportions of QCMT and SCMT cells across each cluster (right). (E) Feature plots of representative proliferation and senescence‐associated genes across clusters. (F) Heatmap of pathway activities across clusters ( Z ‐score normalized). (G) UMAP trajectory analysis using Slingshot identifies four lineages with distinct terminal clusters, including a senescence‐resistant endpoint. Trajectory lines indicate senescence progression, and clusters are colored by pseudotime. (H, I) Boxplots of DNA repair (H) and SASP‐related gene set scores (I) across clusters (Kruskal–Wallis two‐sided test with pairwise Wilcoxon rank‐sum test; adjusted p‐values as shown). (J) Enriched pathways categorized into non‐senescent, intermediate, and fully senescent states. p‐values were calculated using a hypergeometric distribution. (K) Heatmap displaying temporally regulated the top 500 genes identified through tradeSeq along the pseudotime trajectory for lineage 4 in secondary senescence (hypergeometric distribution; p < 0.05).

Techniques: Biomarker Discovery, Two Tailed Test, Enzyme-linked Immunosorbent Assay

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