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Stn1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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stn1 - by Bioz Stars, 2026-11

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1) Product Images from "CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells"

Article Title: CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells

Journal: iScience

doi: 10.1016/j.isci.2026.114646

Figure Legend Snippet: Enrichment of replication stress-associated proteins at CTCF/cohesin-binding sites (A) ChIP-seq signal profile of MRE11 in Mid S HeLa cells plotted across a ±5 kb window centered at CBSs from Mid S HeLa (maroon), CTCF unbound sites (sky blue), and random genomic regions (yellow). A total of 26,948 sites were in each category. The heatmap (on the right) represents the ChIP-seq signal for each site, and the profile plot (on the left) represents the average signal across all sites. (B) Similarly, the ChIP-seq profile of STN1 in Mid S upon HU treatment (from Chastain et al. ) plotted surrounding CBSs and control sites (±5 kb). (C and D) ChIP-seq signals of (C) MRE11 and (D) STN1 (+HU) in Mid S phase plotted surrounding CBSs (maroon; 26,948 sites), CTCF-alone sites (gray; 24,636 sites), and RAD21-alone sites (green; 9,135 sites). (E) MRE11 profile at CBSs based on CTCF and RAD21 binding strength. Light red: CBSs with both CTCF and RAD21 low-binding strength (4,694 sites). Dark red: CBSs with both CTCF and RAD21 high-binding strength (4,775 sites). (F) STN1(+HU) occupancy in the Mid S phase at CTCF/RAD21 low- or high-binding CBSs spanning a ±5 kb window.

Techniques Used: Binding Assay, ChIP-sequencing, Control

Figure Legend Snippet: Replication stress and DNA damage response at CTCF/cohesin-binding sites in normal cells (A–D) ChIP-seq signal profile and heatmap of (A) MRE11, (B) STN1+HU 3h, (C) γH2AX (normalized with H2AX), and (D) RAD51 in the Mid S phase of HeLa cells plotted at CBSs shared between HeLa and normal cells (H1, IMR90, and RPE1 cells) (12,517 sites) and HeLa-specific CBSs (2,293 sites) and normal-specific sites (13,702). For the γH2AX signal ±10 kb flanks were considered, while for others the signal is plotted at ±5 kb regions. (E–H) ChIP-qPCR plots of (E) MRE11, (F) FANCD2, (G) γH2AX, and (H) RAD51 in Mid S synchronized hTERT RPE-1 cells at CBSs and CTCF-unbound sites. The y axis (fold enrichment over beads) indicates the % input in immunoprecipitation divided by that of beads. The bar represents the mean value from three replicates, and the error bar represents the standard error of the mean. Statistical significance was determined by using a two-sided Mann-Whitney U test.

Techniques Used: Binding Assay, ChIP-sequencing, ChIP-qPCR, Immunoprecipitation, MANN-WHITNEY

Enrichment of somatic mutations at CBSs in STN1/MRE11-deleted tumors (A and B) Mutation rate plotted at the ±1 kb region of CBSs Mid S and control sites (CTCF unbound, CTCF-alone, and RAD21-alone sites) in stomach adenocarcinoma samples with (A) both MRE11 and STN1 wild type (No. of samples, N = 38) and (B) both MRE11 and STN1 deletion (No. of samples, N = 4). p -values were calculated by using G-test. (C) Mutation fold change at CBSs ( ±20 bp) core in tumor samples with either MRE11 or STN1 deletion (or both deletion) relative to mutation fold change in MRE11 and STN1 wild-type samples across different tumor types. The statistical difference was calculated by using the Fisher exact test. p -value annotation legend ∗∗: 0.001 < p ≤ 0.01, ∗∗∗∗: p < 0.0001. (D) Mutation fold change at CBSs ( ±20 bp) core stratified based on the CTCF and RAD21 binding strength. On the x axis, the high binding represents CBSs with both CTCF and RAD21 strong binding and low binding represents CBSs with both CTCF and RAD21 weak binding. The statistical difference was calculated by using the Fisher exact test. p -value annotation legend ∗: 0.01 < p ≤ 0.05, ∗∗: 0.001 < p ≤ 0.01, ∗∗∗: 0.0001 < p ≤ 0.001, ∗∗∗∗: p < 0.0001.

Figure Legend Snippet: Enrichment of somatic mutations at CBSs in STN1/MRE11-deleted tumors (A and B) Mutation rate plotted at the ±1 kb region of CBSs Mid S and control sites (CTCF unbound, CTCF-alone, and RAD21-alone sites) in stomach adenocarcinoma samples with (A) both MRE11 and STN1 wild type (No. of samples, N = 38) and (B) both MRE11 and STN1 deletion (No. of samples, N = 4). p -values were calculated by using G-test. (C) Mutation fold change at CBSs ( ±20 bp) core in tumor samples with either MRE11 or STN1 deletion (or both deletion) relative to mutation fold change in MRE11 and STN1 wild-type samples across different tumor types. The statistical difference was calculated by using the Fisher exact test. p -value annotation legend ∗∗: 0.001 < p ≤ 0.01, ∗∗∗∗: p < 0.0001. (D) Mutation fold change at CBSs ( ±20 bp) core stratified based on the CTCF and RAD21 binding strength. On the x axis, the high binding represents CBSs with both CTCF and RAD21 strong binding and low binding represents CBSs with both CTCF and RAD21 weak binding. The statistical difference was calculated by using the Fisher exact test. p -value annotation legend ∗: 0.01 < p ≤ 0.05, ∗∗: 0.001 < p ≤ 0.01, ∗∗∗: 0.0001 < p ≤ 0.001, ∗∗∗∗: p < 0.0001.

Techniques Used: Mutagenesis, Control, Binding Assay

Schematic model for the possible mechanism underlying elevated somatic mutations at CBSs in cancers upon MRE11 and STN1 deletion At CTCF-only bound sites, the replication fork progresses without any constraints and undergoes faithful replication, thus preventing the enrichment of somatic mutations at these sites, whereas cohesin-only bound sites are enriched with DNA sequence susceptible to genomic instability and replication stalling. This can lead to error-prone replication; however, faithful repair post replication prevents the enrichment of somatic mutations at these sites. However, at CTCF/cohesin-binding sites (CBSs), CTCF and cohesin co-binding-induced stress can lead to replication stalling and error-prone replication. Moreover, the immediate re-occupancy of CTCF post replication at these sites could interfere with mismatch recognition and repair, leading to an elevated mutation rate at CBSs.

Figure Legend Snippet: Schematic model for the possible mechanism underlying elevated somatic mutations at CBSs in cancers upon MRE11 and STN1 deletion At CTCF-only bound sites, the replication fork progresses without any constraints and undergoes faithful replication, thus preventing the enrichment of somatic mutations at these sites, whereas cohesin-only bound sites are enriched with DNA sequence susceptible to genomic instability and replication stalling. This can lead to error-prone replication; however, faithful repair post replication prevents the enrichment of somatic mutations at these sites. However, at CTCF/cohesin-binding sites (CBSs), CTCF and cohesin co-binding-induced stress can lead to replication stalling and error-prone replication. Moreover, the immediate re-occupancy of CTCF post replication at these sites could interfere with mismatch recognition and repair, leading to an elevated mutation rate at CBSs.

Techniques Used: Sequencing, Binding Assay, Mutagenesis

Cell-Signaling:

Article Title: 53BP1/Rif1/Shieldin counteract DSB resection through CST/Polα-dependent fill-in
Article Snippet: .. IF for myc-tagged RPA32 or Ctc1 (mouse monoclonal, 9B11 or rabbit monoclonal, 71D10, Cell Signaling Technology), HA-tagged Stn1 (3724, Cell Signaling Technology), endogenous Polα (sc-137021, Santa Cruz), and 53BP1 (612522, BD Biosciences) was carried out using the cytoskeleton extraction protocol . ..

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Journal: iScience

Article Title: CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells

doi: 10.1016/j.isci.2026.114646

Figure Lengend Snippet: Enrichment of replication stress-associated proteins at CTCF/cohesin-binding sites (A) ChIP-seq signal profile of MRE11 in Mid S HeLa cells plotted across a ±5 kb window centered at CBSs from Mid S HeLa (maroon), CTCF unbound sites (sky blue), and random genomic regions (yellow). A total of 26,948 sites were in each category. The heatmap (on the right) represents the ChIP-seq signal for each site, and the profile plot (on the left) represents the average signal across all sites. (B) Similarly, the ChIP-seq profile of STN1 in Mid S upon HU treatment (from Chastain et al. ) plotted surrounding CBSs and control sites (±5 kb). (C and D) ChIP-seq signals of (C) MRE11 and (D) STN1 (+HU) in Mid S phase plotted surrounding CBSs (maroon; 26,948 sites), CTCF-alone sites (gray; 24,636 sites), and RAD21-alone sites (green; 9,135 sites). (E) MRE11 profile at CBSs based on CTCF and RAD21 binding strength. Light red: CBSs with both CTCF and RAD21 low-binding strength (4,694 sites). Dark red: CBSs with both CTCF and RAD21 high-binding strength (4,775 sites). (F) STN1(+HU) occupancy in the Mid S phase at CTCF/RAD21 low- or high-binding CBSs spanning a ±5 kb window.

Article Snippet: STN1 (a part of the human CST: CTC1-STN1-TEN1 complex) is known to protect the stalled replication fork from excessive MRE11-mediated degradation.

Techniques: Binding Assay, ChIP-sequencing, Control

Journal: iScience

Article Title: CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells

doi: 10.1016/j.isci.2026.114646

Figure Lengend Snippet: Replication stress and DNA damage response at CTCF/cohesin-binding sites in normal cells (A–D) ChIP-seq signal profile and heatmap of (A) MRE11, (B) STN1+HU 3h, (C) γH2AX (normalized with H2AX), and (D) RAD51 in the Mid S phase of HeLa cells plotted at CBSs shared between HeLa and normal cells (H1, IMR90, and RPE1 cells) (12,517 sites) and HeLa-specific CBSs (2,293 sites) and normal-specific sites (13,702). For the γH2AX signal ±10 kb flanks were considered, while for others the signal is plotted at ±5 kb regions. (E–H) ChIP-qPCR plots of (E) MRE11, (F) FANCD2, (G) γH2AX, and (H) RAD51 in Mid S synchronized hTERT RPE-1 cells at CBSs and CTCF-unbound sites. The y axis (fold enrichment over beads) indicates the % input in immunoprecipitation divided by that of beads. The bar represents the mean value from three replicates, and the error bar represents the standard error of the mean. Statistical significance was determined by using a two-sided Mann-Whitney U test.

Article Snippet: STN1 (a part of the human CST: CTC1-STN1-TEN1 complex) is known to protect the stalled replication fork from excessive MRE11-mediated degradation.

Techniques: Binding Assay, ChIP-sequencing, ChIP-qPCR, Immunoprecipitation, MANN-WHITNEY

Journal: iScience

Article Title: CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells

doi: 10.1016/j.isci.2026.114646

Figure Lengend Snippet: Enrichment of somatic mutations at CBSs in STN1/MRE11-deleted tumors (A and B) Mutation rate plotted at the ±1 kb region of CBSs Mid S and control sites (CTCF unbound, CTCF-alone, and RAD21-alone sites) in stomach adenocarcinoma samples with (A) both MRE11 and STN1 wild type (No. of samples, N = 38) and (B) both MRE11 and STN1 deletion (No. of samples, N = 4). p -values were calculated by using G-test. (C) Mutation fold change at CBSs ( ±20 bp) core in tumor samples with either MRE11 or STN1 deletion (or both deletion) relative to mutation fold change in MRE11 and STN1 wild-type samples across different tumor types. The statistical difference was calculated by using the Fisher exact test. p -value annotation legend ∗∗: 0.001 < p ≤ 0.01, ∗∗∗∗: p < 0.0001. (D) Mutation fold change at CBSs ( ±20 bp) core stratified based on the CTCF and RAD21 binding strength. On the x axis, the high binding represents CBSs with both CTCF and RAD21 strong binding and low binding represents CBSs with both CTCF and RAD21 weak binding. The statistical difference was calculated by using the Fisher exact test. p -value annotation legend ∗: 0.01 < p ≤ 0.05, ∗∗: 0.001 < p ≤ 0.01, ∗∗∗: 0.0001 < p ≤ 0.001, ∗∗∗∗: p < 0.0001.

Article Snippet: STN1 (a part of the human CST: CTC1-STN1-TEN1 complex) is known to protect the stalled replication fork from excessive MRE11-mediated degradation.

Techniques: Mutagenesis, Control, Binding Assay

Journal: iScience

Article Title: CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells

doi: 10.1016/j.isci.2026.114646

Figure Lengend Snippet: Schematic model for the possible mechanism underlying elevated somatic mutations at CBSs in cancers upon MRE11 and STN1 deletion At CTCF-only bound sites, the replication fork progresses without any constraints and undergoes faithful replication, thus preventing the enrichment of somatic mutations at these sites, whereas cohesin-only bound sites are enriched with DNA sequence susceptible to genomic instability and replication stalling. This can lead to error-prone replication; however, faithful repair post replication prevents the enrichment of somatic mutations at these sites. However, at CTCF/cohesin-binding sites (CBSs), CTCF and cohesin co-binding-induced stress can lead to replication stalling and error-prone replication. Moreover, the immediate re-occupancy of CTCF post replication at these sites could interfere with mismatch recognition and repair, leading to an elevated mutation rate at CBSs.

Article Snippet: STN1 (a part of the human CST: CTC1-STN1-TEN1 complex) is known to protect the stalled replication fork from excessive MRE11-mediated degradation.

Techniques: Sequencing, Binding Assay, Mutagenesis

(A) Frequency of CST gene alterations observed in cutaneous melanoma. Well-known melanoma-associated genes are shown for comparison. Data are derived from TCGA PanCancer Atlas Skin Cutaneous Melanoma dataset. (B) CTC1, STN1, TEN1 expression is significantly downregulated in skin cutaneous melanoma. Analysis was performed using TNMplot based on RNA-seq data from paired tumor and normal samples. P : Mann-Whitney U test. N : number of samples.

Journal: PLOS One

Article Title: In vivo investigation of STN1 downregulation in melanoma formation in adult mice following UV irradiation

doi: 10.1371/journal.pone.0326647

Figure Lengend Snippet: (A) Frequency of CST gene alterations observed in cutaneous melanoma. Well-known melanoma-associated genes are shown for comparison. Data are derived from TCGA PanCancer Atlas Skin Cutaneous Melanoma dataset. (B) CTC1, STN1, TEN1 expression is significantly downregulated in skin cutaneous melanoma. Analysis was performed using TNMplot based on RNA-seq data from paired tumor and normal samples. P : Mann-Whitney U test. N : number of samples.

Article Snippet: Sections were then incubated with a primary antibody against Stn1 (1:100, Santa Cruz, 376450) and S100B (1:5,000, ProteinTech, 15146-AP) overnight at 4°C.

Techniques: Comparison, Derivative Assay, Expressing, RNA Sequencing, MANN-WHITNEY

(A) Scheme of STN1 cKO. The murine STN1 gene contains 10 exons. Only exons 1-4 are shown. The ATG start codon is located in exon 2 (red). Exon 1 is a non-coding exon. Triangles: loxP sites. (B) Genotyping results of STN1 F/F , Tyr::CreER T2 and Braf V600E alleles in mice used in this study.

Journal: PLOS One

Article Title: In vivo investigation of STN1 downregulation in melanoma formation in adult mice following UV irradiation

doi: 10.1371/journal.pone.0326647

Figure Lengend Snippet: (A) Scheme of STN1 cKO. The murine STN1 gene contains 10 exons. Only exons 1-4 are shown. The ATG start codon is located in exon 2 (red). Exon 1 is a non-coding exon. Triangles: loxP sites. (B) Genotyping results of STN1 F/F , Tyr::CreER T2 and Braf V600E alleles in mice used in this study.

Article Snippet: Sections were then incubated with a primary antibody against Stn1 (1:100, Santa Cruz, 376450) and S100B (1:5,000, ProteinTech, 15146-AP) overnight at 4°C.

Techniques:

(A) Scheme of TAM treatment and UV exposure. (B) IHC of Stn1 in skin tissue sections from Tyr::CreER T2 ; STN1 F/F and wild-type animals. Red arrows point to Stn1 staining in hair follicles of the control sample. Inserts show amplified images of the boxed areas. (C) Representative image of melanoma (dark speckles) developed on the back of the shaved skin in Tyr::CreER T2 ; Braf V600E mice. (D) Kaplan-Meier curve showing melanoma-free survival in UV-irradiated animals. (E) Representative H&E staining of skin tissues collected from mice. Inserts show amplified images of the boxed areas. (F) Representative IHC staining of S100B in skin tissues collected from mice. Inserts show amplified images of the boxed areas. Red arrows point to S100B positively stained cells. (G) Melanoma formation frequency in UV-irradiated animals. P : two-sided Fisher exact tests. The number of animals in each group is shown below the plot.

Journal: PLOS One

Article Title: In vivo investigation of STN1 downregulation in melanoma formation in adult mice following UV irradiation

doi: 10.1371/journal.pone.0326647

Figure Lengend Snippet: (A) Scheme of TAM treatment and UV exposure. (B) IHC of Stn1 in skin tissue sections from Tyr::CreER T2 ; STN1 F/F and wild-type animals. Red arrows point to Stn1 staining in hair follicles of the control sample. Inserts show amplified images of the boxed areas. (C) Representative image of melanoma (dark speckles) developed on the back of the shaved skin in Tyr::CreER T2 ; Braf V600E mice. (D) Kaplan-Meier curve showing melanoma-free survival in UV-irradiated animals. (E) Representative H&E staining of skin tissues collected from mice. Inserts show amplified images of the boxed areas. (F) Representative IHC staining of S100B in skin tissues collected from mice. Inserts show amplified images of the boxed areas. Red arrows point to S100B positively stained cells. (G) Melanoma formation frequency in UV-irradiated animals. P : two-sided Fisher exact tests. The number of animals in each group is shown below the plot.

Article Snippet: Sections were then incubated with a primary antibody against Stn1 (1:100, Santa Cruz, 376450) and S100B (1:5,000, ProteinTech, 15146-AP) overnight at 4°C.

Techniques: Staining, Control, Amplification, Irradiation, Immunohistochemistry

(A) Representative images of γH2AX IHC staining of melanoma tissues collected from Stn1 F/F and Tyr::CreERT2 Stn1 F/F mice. γH2AX signal intensity was quantified using ImageJ and plotted. (B) Representative images of CPD IHC staining of melanoma tissues collected from Stn1 F/F and Tyr::CreERT2 Stn1 F/F mice. CPD signal intensity was quantified using ImageJ and plotted.

Journal: PLOS One

Article Title: In vivo investigation of STN1 downregulation in melanoma formation in adult mice following UV irradiation

doi: 10.1371/journal.pone.0326647

Figure Lengend Snippet: (A) Representative images of γH2AX IHC staining of melanoma tissues collected from Stn1 F/F and Tyr::CreERT2 Stn1 F/F mice. γH2AX signal intensity was quantified using ImageJ and plotted. (B) Representative images of CPD IHC staining of melanoma tissues collected from Stn1 F/F and Tyr::CreERT2 Stn1 F/F mice. CPD signal intensity was quantified using ImageJ and plotted.

Article Snippet: Sections were then incubated with a primary antibody against Stn1 (1:100, Santa Cruz, 376450) and S100B (1:5,000, ProteinTech, 15146-AP) overnight at 4°C.

Techniques: Immunohistochemistry

(A) Western blot of STN1 levels in HeLa iCas9 sgSTN1 cells, as indicated. Actinin serves as a loading control. DOX=Doxycycline. (B) Growth curve analysis of STN1 KO and control cells. D=day after DOX addition. n=3 independent, biological replicates. (C-D) Flow cytometry analysis of STN1 KO cells. (C) Representative histograms of STN1 KO and control (-DOX) cells. Left, histograms of DNA content versus cell count. Right, DNA content versus EdU intensity. (D) Percentage of G2/M cells over time in STN1 KO cells. n=3 independent, biological replicates. Average values in the graphs indicate the mean and error bars denote ±s.e.m. P -values were calculated by a two-tailed, unpaired t -test.

Journal: bioRxiv

Article Title: Conditional deletion of human STN1 leads to telomere dysfunction and telomerase-dependent genome instability and proliferation defects

doi: 10.1101/2025.08.06.669015

Figure Lengend Snippet: (A) Western blot of STN1 levels in HeLa iCas9 sgSTN1 cells, as indicated. Actinin serves as a loading control. DOX=Doxycycline. (B) Growth curve analysis of STN1 KO and control cells. D=day after DOX addition. n=3 independent, biological replicates. (C-D) Flow cytometry analysis of STN1 KO cells. (C) Representative histograms of STN1 KO and control (-DOX) cells. Left, histograms of DNA content versus cell count. Right, DNA content versus EdU intensity. (D) Percentage of G2/M cells over time in STN1 KO cells. n=3 independent, biological replicates. Average values in the graphs indicate the mean and error bars denote ±s.e.m. P -values were calculated by a two-tailed, unpaired t -test.

Article Snippet: Primary: OBFC1 (STN1) (Novus, NBP2-01006), Actinin (Santa Cruz, sc17829), pH3 S10 (Cell Signaling, 9706), RPA32 (Abcam, ab16850), and γH2AX (Bethyl, A300-081A; Abcam, ab81299).

Techniques: Western Blot, Control, Flow Cytometry, Cell Counting, Two Tailed Test

(A) Representative image of RPA-γH2AX foci. STN1 KO image is from day 12 after DOX addition. (B-C) Analysis of foci in STN1 KO and control (-DOX) cells. Percentage of nuclei displaying 3 or more RPA (B) or RPA-γH2AX foci (C). n=3 independent, biological replicates. Average values in the graphs indicate the mean and error bars denote ±s.e.m. P -values were calculated by a two-tailed, unpaired t -test. DOX=Doxycycline. D=day after DOX addition.

Journal: bioRxiv

Article Title: Conditional deletion of human STN1 leads to telomere dysfunction and telomerase-dependent genome instability and proliferation defects

doi: 10.1101/2025.08.06.669015

Figure Lengend Snippet: (A) Representative image of RPA-γH2AX foci. STN1 KO image is from day 12 after DOX addition. (B-C) Analysis of foci in STN1 KO and control (-DOX) cells. Percentage of nuclei displaying 3 or more RPA (B) or RPA-γH2AX foci (C). n=3 independent, biological replicates. Average values in the graphs indicate the mean and error bars denote ±s.e.m. P -values were calculated by a two-tailed, unpaired t -test. DOX=Doxycycline. D=day after DOX addition.

Article Snippet: Primary: OBFC1 (STN1) (Novus, NBP2-01006), Actinin (Santa Cruz, sc17829), pH3 S10 (Cell Signaling, 9706), RPA32 (Abcam, ab16850), and γH2AX (Bethyl, A300-081A; Abcam, ab81299).

Techniques: Control, Two Tailed Test

(A) Western blot of STN1 and Flag-STN1 levels, as indicated. KO+Flag-STN1 denotes STN1 KO cells expressing Flag-STN1. Actinin serves as a loading control. (B) Percentage of nuclei displaying 3 or more RPA foci on day 15 after DOX addition. n=3 independent, biological replicates. (C) Growth curve analysis, as indicated. n=3 independent, biological replicates. (D) Percentage of G2/M cells determined by flow cytometry on day 15 after DOX addition. n=4 independent, biological replicates. Average values in the graphs indicate the mean and error bars denote ±s.e.m. P -values were calculated by a two-tailed, unpaired t -test. DOX=Doxycycline.

Journal: bioRxiv

Article Title: Conditional deletion of human STN1 leads to telomere dysfunction and telomerase-dependent genome instability and proliferation defects

doi: 10.1101/2025.08.06.669015

Figure Lengend Snippet: (A) Western blot of STN1 and Flag-STN1 levels, as indicated. KO+Flag-STN1 denotes STN1 KO cells expressing Flag-STN1. Actinin serves as a loading control. (B) Percentage of nuclei displaying 3 or more RPA foci on day 15 after DOX addition. n=3 independent, biological replicates. (C) Growth curve analysis, as indicated. n=3 independent, biological replicates. (D) Percentage of G2/M cells determined by flow cytometry on day 15 after DOX addition. n=4 independent, biological replicates. Average values in the graphs indicate the mean and error bars denote ±s.e.m. P -values were calculated by a two-tailed, unpaired t -test. DOX=Doxycycline.

Article Snippet: Primary: OBFC1 (STN1) (Novus, NBP2-01006), Actinin (Santa Cruz, sc17829), pH3 S10 (Cell Signaling, 9706), RPA32 (Abcam, ab16850), and γH2AX (Bethyl, A300-081A; Abcam, ab81299).

Techniques: Western Blot, Expressing, Control, Flow Cytometry, Two Tailed Test

(A) Representative image of an anaphase bridge (indicated by the arrow) in STN1 KO cells. (B-C) Percentage of anaphase bridges in STN1 KO and control (-DOX) cells between days 5-15 (B) or with expression of exogenous Flag-STN1 on day 15 (C). n=≥3 independent, biological replicates. (D) Representative image of micronuclei (indicated by the arrows) in the STN1 KO cells. (E-F) Percentage of cells with micronuclei in STN1 KO and control cells between days 5-15 (E) or with expression of exogenous Flag-STN1 on day 15 (F). n=≥3 independent, biological replicates. Average values in the graphs indicate the mean and error bars denote ±s.e.m. P -values were calculated by a two-tailed, unpaired t -test. DOX=Doxycycline. D=day after DOX addition.

Journal: bioRxiv

Article Title: Conditional deletion of human STN1 leads to telomere dysfunction and telomerase-dependent genome instability and proliferation defects

doi: 10.1101/2025.08.06.669015

Figure Lengend Snippet: (A) Representative image of an anaphase bridge (indicated by the arrow) in STN1 KO cells. (B-C) Percentage of anaphase bridges in STN1 KO and control (-DOX) cells between days 5-15 (B) or with expression of exogenous Flag-STN1 on day 15 (C). n=≥3 independent, biological replicates. (D) Representative image of micronuclei (indicated by the arrows) in the STN1 KO cells. (E-F) Percentage of cells with micronuclei in STN1 KO and control cells between days 5-15 (E) or with expression of exogenous Flag-STN1 on day 15 (F). n=≥3 independent, biological replicates. Average values in the graphs indicate the mean and error bars denote ±s.e.m. P -values were calculated by a two-tailed, unpaired t -test. DOX=Doxycycline. D=day after DOX addition.

Article Snippet: Primary: OBFC1 (STN1) (Novus, NBP2-01006), Actinin (Santa Cruz, sc17829), pH3 S10 (Cell Signaling, 9706), RPA32 (Abcam, ab16850), and γH2AX (Bethyl, A300-081A; Abcam, ab81299).

Techniques: Control, Expressing, Two Tailed Test

Cells were treated with a telomerase inhibitor (BIBR) or DMSO starting with the addition of DOX on day 0 to the sgSTN1 cells. The control cells were also treated with BIBR or DMSO across the same timeframe. (A-B) Percentage of nuclei with 3 or more RPA (A) or RPA-γH2AX (B) foci in STN1 KO or control cells with or without BIBR treatment. n=3 independent, biological replicates. (C-D) Percentage of micronuclei (C) or anaphase bridges (D) on day 15 after DOX addition with and without BIBR treatment. n=4 independent, biological replicates. (E) Growth curve analysis, as indicated. n=3 independent, biological replicates. Average values in the graphs indicate the mean and error bars denote ±s.e.m. P -values were calculated by a two-tailed, unpaired t -test. DOX=Doxycycline. D=day after DOX addition.

Journal: bioRxiv

Article Title: Conditional deletion of human STN1 leads to telomere dysfunction and telomerase-dependent genome instability and proliferation defects

doi: 10.1101/2025.08.06.669015

Figure Lengend Snippet: Cells were treated with a telomerase inhibitor (BIBR) or DMSO starting with the addition of DOX on day 0 to the sgSTN1 cells. The control cells were also treated with BIBR or DMSO across the same timeframe. (A-B) Percentage of nuclei with 3 or more RPA (A) or RPA-γH2AX (B) foci in STN1 KO or control cells with or without BIBR treatment. n=3 independent, biological replicates. (C-D) Percentage of micronuclei (C) or anaphase bridges (D) on day 15 after DOX addition with and without BIBR treatment. n=4 independent, biological replicates. (E) Growth curve analysis, as indicated. n=3 independent, biological replicates. Average values in the graphs indicate the mean and error bars denote ±s.e.m. P -values were calculated by a two-tailed, unpaired t -test. DOX=Doxycycline. D=day after DOX addition.

Article Snippet: Primary: OBFC1 (STN1) (Novus, NBP2-01006), Actinin (Santa Cruz, sc17829), pH3 S10 (Cell Signaling, 9706), RPA32 (Abcam, ab16850), and γH2AX (Bethyl, A300-081A; Abcam, ab81299).

Techniques: Control, Two Tailed Test

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stn1 (Cell Signaling Technology Inc)

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