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rabbit anti trf2 (Novus Biologicals)

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Novus Biologicals rabbit anti trf2
Rabbit Anti Trf2, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 95/100, based on 130 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rabbit+trf2/TRF-2+Antibody+-+BSA+Free/pm41712379-430-4-5
Average 95 stars, based on 130 article reviews

rabbit anti trf2 - by Bioz Stars, 2026-11

95/100 stars

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Immunoprecipitation:

Article Title: The C-Terminal Extension Unique to the Long Isoform of the Shelterin Component TIN2 Enhances Its Interaction with TRF2 in a Phosphorylation- and Dyskeratosis Congenita Cluster-Dependent Fashion
Article Snippet: Cellular debris was pelleted by 317 centrifugation at 4 ̊C and 20,000 g for 10 minutes, and the protein concentration 318 assessed using the BCA protein assay kit (Pierce). .. For immunoprecipitation 600 μg of 319 the lysate was incubated with the corresponding antibodies (3 μg) overnight at 4 C: 320 rabbit-TRF2 (Novus, NB110-57130), rabbit -TRF1 (Abcam, ab1423), rabbit IgG 321 (Santa Cruz). .. The next day, 45 μl of protein G magnetic beads (Pierce) were added and 322 after 2 hours, the beads were washed 2X in RIPA buffer, 4X in wash buffer (100 mM 323 Tris-HCl pH 8.5, 500 mM LiCl, 1% NP-40, 1% sodium deoxycholate) and another 2X in 324 RIPA buffer.

Article Title: TRF2 cooperates with CTCF for controlling the oncomiR-193b-3p in colorectal cancer.
Article Snippet: .. The antibodies used for the immunoprecipitation are: rabbit TRF2 (NB110-57130, Novus), rabbit CTCF (C15410210-50, Diagenode), IgG Rabbit (Bethyl). ..

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other:

Article Title: Loss of SLX4IP leads to common fragile site instability and compromises DNA interstrand crosslink repair in vivo
Article Snippet: High-content image analysis and foci counts were performed with software Olympus ScanR Analysis 3.2 and exported to Tibco Spotfire v.10.3 for appropriate gating.

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Effect of DISS on telomere. ( A ) The changes in telomerase content after treatment with 0, 1, 3, 10 μM DISS or 10 μM RES. ( B ) Relative telomere length of 3T3 cells after treatment with 0, 1, 3, 10 μM DISS or 10 μM AST. ( C , D ) Effects of 1, 3, 10 μM DISS or 10 μM RES on EST1 , EST2 genes at 24 and 48 h. ( E ) Effects of 0, 1, 3, 10 μM DISS or 10 μM AST on TRF2 protein expressions and digital results. ( F ) Effects of 0, 1, 3, 10 μM DISS or 10 μM AST on RAP1 protein expressions and the digital results. qPCR was performed for 40 cycles. For qPCR, each RNA sample was subjected to three technical replicates ( n = 3). Western blot analysis was performed with three biological replicates. ( n = 3). *, ** and *** represent significant differences at p < 0.05, p < 0.01, and p < 0.001 compared with the negative control group, respectively. # and ### represent significant differences at p < 0.05, p < 0.001 compared with the negative control group for 48 h, respectively.

Journal: Antioxidants

Article Title: 3,6′-Disinapoyl Sucrose from Polygalae Radix Exerts Anti-Aging Effects via Modification of Telomeres, SIRT1/p53/p21 Pathway, Oxidative Stress and Autophagy

doi: 10.3390/antiox15030313

Figure Lengend Snippet: Effect of DISS on telomere. ( A ) The changes in telomerase content after treatment with 0, 1, 3, 10 μM DISS or 10 μM RES. ( B ) Relative telomere length of 3T3 cells after treatment with 0, 1, 3, 10 μM DISS or 10 μM AST. ( C , D ) Effects of 1, 3, 10 μM DISS or 10 μM RES on EST1 , EST2 genes at 24 and 48 h. ( E ) Effects of 0, 1, 3, 10 μM DISS or 10 μM AST on TRF2 protein expressions and digital results. ( F ) Effects of 0, 1, 3, 10 μM DISS or 10 μM AST on RAP1 protein expressions and the digital results. qPCR was performed for 40 cycles. For qPCR, each RNA sample was subjected to three technical replicates ( n = 3). Western blot analysis was performed with three biological replicates. ( n = 3). *, ** and *** represent significant differences at p < 0.05, p < 0.01, and p < 0.001 compared with the negative control group, respectively. # and ### represent significant differences at p < 0.05, p < 0.001 compared with the negative control group for 48 h, respectively.

Article Snippet: The first antibodies used in this experiment were as follows: SIRT1 antibody (Cell Signaling Technology, Shanghai, China, #9475, 1:1000), GFP antibody (Wuhan Sanying Biotechnology Co., Ltd., Wuhan, China, 50430-2-AP, 1:1000), p53 antibody (Hangzhou Huaan Biotechnology Co., Ltd., Hangzhou, China, HA722074, 1:1000), p21 antibody (Hangzhou Huaan Biotechnology Co., Ltd., Hangzhou, China, HA722065, 1:1000), TRF2 antibody (Cell Signaling Technology, Shanghai, China, #13136, 1:1000), and RAP1 antibody (Cell Signaling Technology, Shanghai, China, #5433, 1:1000), and β -actin antibody (Hangzhou Daige Biotech Co., Ltd., Hangzhou, China, #db13986, 1:1000).

Techniques: Western Blot, Negative Control

Regulation of BLM-LI and TSE-LI by IL-17A. ( A ) Lung sections of WT mice exposed to saline or BLM for 24–72 h were subjected to IHC staining for IL-17A antigen ( i ). AECs isolated from WT and IL-17A-deficient mice exposed to saline or BLM were analyzed for apoptosis and Sirt1 expression by Western blotting (WB) three days later ( ii ). Lung sections of WT and IL-17A −/− mice exposed to saline or BLM were subjected to Masson’s trichrome staining 21 days later ( iii ). Whole lung homogenates of WT and IL-17A −/− mice exposed to saline or BLM as in were analyzed for total HYP content ( iv ) or for Col-1 and FN by WB 21 days after BLM ( v ). ( B ) WT, p53 −/− and PAI-1 −/− mice were kept in ambient air or exposed to passive TS for 20 weeks. Total lung homogenates of control mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice were analyzed for IL-17A and IL-17RA protein by WB ( i ). Total RNA from mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice was analyzed for IL-17A mRNA ( ii ). AECs from TSE WT and IL-17A −/− mice were analyzed for p53, ACp53, cleaved (Cl.) caspase-3/caspase-3 and Sirt1 by WB ( iii ). AECs from lungs of IL-17A −/− mice kept in ambient air or TSE, as well as mice treated with or without CSP7 or CP, were analyzed for telomere length by qPCR ( iv ). AECs from lungs of IL-17A −/− mice treated as in ( B(iv )) were immunoblotted for the listed proteins ( v ). Lung sections of IL-17A −/− mice treated as in ( B ( iv )) were subjected to IHC for telomere binding shelterin complex (TRF1 and TRF2) proteins ( vi ).

Journal: International Journal of Molecular Sciences

Article Title: Interleukin-17A Orchestrates Lung Injury and Remodeling Through p53 and uPA System Crosstalk

doi: 10.3390/ijms27041841

Figure Lengend Snippet: Regulation of BLM-LI and TSE-LI by IL-17A. ( A ) Lung sections of WT mice exposed to saline or BLM for 24–72 h were subjected to IHC staining for IL-17A antigen ( i ). AECs isolated from WT and IL-17A-deficient mice exposed to saline or BLM were analyzed for apoptosis and Sirt1 expression by Western blotting (WB) three days later ( ii ). Lung sections of WT and IL-17A −/− mice exposed to saline or BLM were subjected to Masson’s trichrome staining 21 days later ( iii ). Whole lung homogenates of WT and IL-17A −/− mice exposed to saline or BLM as in were analyzed for total HYP content ( iv ) or for Col-1 and FN by WB 21 days after BLM ( v ). ( B ) WT, p53 −/− and PAI-1 −/− mice were kept in ambient air or exposed to passive TS for 20 weeks. Total lung homogenates of control mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice were analyzed for IL-17A and IL-17RA protein by WB ( i ). Total RNA from mice kept in ambient air, TSE WT mice, and p53 −/− or PAI-1 −/− mice was analyzed for IL-17A mRNA ( ii ). AECs from TSE WT and IL-17A −/− mice were analyzed for p53, ACp53, cleaved (Cl.) caspase-3/caspase-3 and Sirt1 by WB ( iii ). AECs from lungs of IL-17A −/− mice kept in ambient air or TSE, as well as mice treated with or without CSP7 or CP, were analyzed for telomere length by qPCR ( iv ). AECs from lungs of IL-17A −/− mice treated as in ( B(iv )) were immunoblotted for the listed proteins ( v ). Lung sections of IL-17A −/− mice treated as in ( B ( iv )) were subjected to IHC for telomere binding shelterin complex (TRF1 and TRF2) proteins ( vi ).

Article Snippet: 12 , TRF2 (D1Y5D) rabbit mAb , CST , 13136S , 1:1000 , 1:500.

Techniques: Saline, Immunohistochemistry, Isolation, Expressing, Western Blot, Staining, Control, Binding Assay

(a) Immunoblot for 53BP1, TRF2 and actin (loading control) in Trf2 F/F 53bp1 −/− MEFs expressing empty vector (EV), full-length wild-type 53BP1 (WT) or its GAR mutants (R→A or R→K), before or 96 h after Cre-mediated Trf2 deletion with Hit&Run Cre. (b) Representative metaphase spreads in the indicated MEFs at 96 h after Cre-mediated Trf2 deletion. Telomeres were detected with Alexa Fluor 488-OO-(TTAGGG) 3 (green), DNA with DAPI (magenta). Arrows indicate telomere fusions. The boxed regions are enlarged in the right row. Scale bar = 10 µm. (c-d) Quantification of telomere fusions shown in (b) at 96 h (c) or 120 h (d) after Cre-mediated Trf2 deletion. Data are presented as median from 3 independent experiments (10 metaphases each). Each data point represents the percentage of telomeres fused in one metaphase, with different shapes indicating the different replicates. Statistical analysis was performed using one-way ANOVA, followed by Tukey’s post hoc test (* P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001).

Journal: bioRxiv

Article Title: The glycine-arginine-rich motif of 53BP1 modulates RNA interactions necessary for its liquid-liquid phase separation during DNA Damage Response

doi: 10.64898/2026.01.30.702603

Figure Lengend Snippet: (a) Immunoblot for 53BP1, TRF2 and actin (loading control) in Trf2 F/F 53bp1 −/− MEFs expressing empty vector (EV), full-length wild-type 53BP1 (WT) or its GAR mutants (R→A or R→K), before or 96 h after Cre-mediated Trf2 deletion with Hit&Run Cre. (b) Representative metaphase spreads in the indicated MEFs at 96 h after Cre-mediated Trf2 deletion. Telomeres were detected with Alexa Fluor 488-OO-(TTAGGG) 3 (green), DNA with DAPI (magenta). Arrows indicate telomere fusions. The boxed regions are enlarged in the right row. Scale bar = 10 µm. (c-d) Quantification of telomere fusions shown in (b) at 96 h (c) or 120 h (d) after Cre-mediated Trf2 deletion. Data are presented as median from 3 independent experiments (10 metaphases each). Each data point represents the percentage of telomeres fused in one metaphase, with different shapes indicating the different replicates. Statistical analysis was performed using one-way ANOVA, followed by Tukey’s post hoc test (* P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001).

Article Snippet: The membrane was blocked in 5% milk in PBS containing 0.1% (v/v) Tween-20 (PBS-T), and immunoblotted using the following antibodies: 53BP1 (ab175933, Abcam), TRF2 (13136, Cell Signaling), β-actin (3700, Cell Signaling), followed by goat anti-rabbit (31460, Invitrogen) or anti-mouse (31430, Invitrogen) IgG-HRP secondary antibodies.

Techniques: Western Blot, Control, Expressing, Plasmid Preparation

Elevated TERF2 expression in AML patients and its correlation with clinicopathological features. (A) Transcriptional expression of TERF2 in AML analyzed using TCGA database. (B) TERF2 mRNA levels quantified by qRT-PCR in PBMCs from 50 AML patients and 35 healthy donors. (C) UMAP of single cells from an AML patient ( GSE116256 ), single-cell profiling reveals distinct expression patterns of TERF2 across cellular subpopulations in AML. (D) Heatmap depicting the average expression level of TERF2 across distinct cell types within the AML sample. (E) Univariate Cox proportional hazards regression analysis comparing survival outcomes between high- and low-TERF2 expression groups. (F) Prognostic accuracy of TERF2 evaluated using ROC curve analysis. (G) The predictive performance of the novel risk stratification model was evaluated through time-dependent ROC curve analysis, with AUC values calculated at 1-, 3-, and 5-year intervals to quantify sensitivity and specificity in AML prognosis. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; AUC, area under the curve; CI, confidence interval; FPR, false positive rate; HR, hazard ratio; PBMCs, peripheral blood mononuclear cells; qRT-PCR, quantitative reverse transcription polymerase chain reaction; ROC, receiver operating characteristic; TCGA, The Cancer Genome Atlas; TPM, transcripts per million; TPR, true positive rate; UMAP, uniform manifold approximation and projection.

Journal: Translational Cancer Research

Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

doi: 10.21037/tcr-2025-1226

Figure Lengend Snippet: Elevated TERF2 expression in AML patients and its correlation with clinicopathological features. (A) Transcriptional expression of TERF2 in AML analyzed using TCGA database. (B) TERF2 mRNA levels quantified by qRT-PCR in PBMCs from 50 AML patients and 35 healthy donors. (C) UMAP of single cells from an AML patient ( GSE116256 ), single-cell profiling reveals distinct expression patterns of TERF2 across cellular subpopulations in AML. (D) Heatmap depicting the average expression level of TERF2 across distinct cell types within the AML sample. (E) Univariate Cox proportional hazards regression analysis comparing survival outcomes between high- and low-TERF2 expression groups. (F) Prognostic accuracy of TERF2 evaluated using ROC curve analysis. (G) The predictive performance of the novel risk stratification model was evaluated through time-dependent ROC curve analysis, with AUC values calculated at 1-, 3-, and 5-year intervals to quantify sensitivity and specificity in AML prognosis. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; AUC, area under the curve; CI, confidence interval; FPR, false positive rate; HR, hazard ratio; PBMCs, peripheral blood mononuclear cells; qRT-PCR, quantitative reverse transcription polymerase chain reaction; ROC, receiver operating characteristic; TCGA, The Cancer Genome Atlas; TPM, transcripts per million; TPR, true positive rate; UMAP, uniform manifold approximation and projection.

Article Snippet: Primary antibodies targeting TERF2 (#13136, 1:500 dilution), CDK4 (#12790, 1:500), CDK6 (#1331, 1:500), and CDKN2A (#80772, 1:500) were commercially obtained from CST (Danvers, MA, USA).

Techniques: Expressing, Quantitative RT-PCR, Reverse Transcription, Polymerase Chain Reaction

Downregulation of TERF2 suppresses AML cells viability and proliferation. (A) qRT-PCR assays analyzed TERF2 mRNA levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (B) Western blot assays detected TERF2 protein levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (C,D) CCK-8 assay showing the viability of NC or TERF2-knockdown MOLM13 cells (C) and THP1 cells (D). (E-H) Flow cytometry assay analyzed cell cycle in NC or TERF2-knockdown MOLM13 cells (E,F) and THP1 cells (G,H). **, P<0.01; ****, P<0.0001; ns, not significant. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; NC, negative control; qRT-PCR, quantitative reverse transcription polymerase chain reaction.

Journal: Translational Cancer Research

Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

doi: 10.21037/tcr-2025-1226

Figure Lengend Snippet: Downregulation of TERF2 suppresses AML cells viability and proliferation. (A) qRT-PCR assays analyzed TERF2 mRNA levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (B) Western blot assays detected TERF2 protein levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (C,D) CCK-8 assay showing the viability of NC or TERF2-knockdown MOLM13 cells (C) and THP1 cells (D). (E-H) Flow cytometry assay analyzed cell cycle in NC or TERF2-knockdown MOLM13 cells (E,F) and THP1 cells (G,H). **, P<0.01; ****, P<0.0001; ns, not significant. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; NC, negative control; qRT-PCR, quantitative reverse transcription polymerase chain reaction.

Techniques: Quantitative RT-PCR, Knockdown, Western Blot, CCK-8 Assay, Flow Cytometry, Cell Counting, Negative Control, Reverse Transcription, Polymerase Chain Reaction

TERF2 deficiency promotes apoptosis in AML cells. (A-D) Flow cytometry assay analyzed apoptosis in NC or TERF2-knockdown MOLM13 cells (A,B) or THP1 cells (C,D). (E-H) Western blot detected cleaved caspase 3 levels of NC or TERF2-knockdown MOLM13 cells (E,F) or THP1 cells (G,H). ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; NC, negative control.

Journal: Translational Cancer Research

Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

doi: 10.21037/tcr-2025-1226

Figure Lengend Snippet: TERF2 deficiency promotes apoptosis in AML cells. (A-D) Flow cytometry assay analyzed apoptosis in NC or TERF2-knockdown MOLM13 cells (A,B) or THP1 cells (C,D). (E-H) Western blot detected cleaved caspase 3 levels of NC or TERF2-knockdown MOLM13 cells (E,F) or THP1 cells (G,H). ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; NC, negative control.

Techniques: Flow Cytometry, Knockdown, Western Blot, Negative Control

TERF2 involved in cuproptosis through E2F pathway in AML. (A) Bar graphs illustrate the associations between TERF2 expression levels and gene hallmark sets in AML patients. (B) GSEA for AML patients with high TERF2 expression in TCGA database. (C-E) Western blot analysis of E2F1, CDK4, CDK6, CDKN2A levels in MOLM13 cells and NB4 cells with or without TERF2 silence. (F,G) MOLM13 (F) and NB4 (G) cells with TERF2 knockdown were treated with specified concentrations of ES-Cu (1:1 ratio) for 48 hours, followed by cell viability assessment using the CCK-8 assay. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; ES-Cu, elesclomol-copper; GSEA, gene set enrichment analysis; IC 50 , half-maximal inhibitory concentration; TCGA, The Cancer Genome Atlas.

Journal: Translational Cancer Research

Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

doi: 10.21037/tcr-2025-1226

Figure Lengend Snippet: TERF2 involved in cuproptosis through E2F pathway in AML. (A) Bar graphs illustrate the associations between TERF2 expression levels and gene hallmark sets in AML patients. (B) GSEA for AML patients with high TERF2 expression in TCGA database. (C-E) Western blot analysis of E2F1, CDK4, CDK6, CDKN2A levels in MOLM13 cells and NB4 cells with or without TERF2 silence. (F,G) MOLM13 (F) and NB4 (G) cells with TERF2 knockdown were treated with specified concentrations of ES-Cu (1:1 ratio) for 48 hours, followed by cell viability assessment using the CCK-8 assay. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; ES-Cu, elesclomol-copper; GSEA, gene set enrichment analysis; IC 50 , half-maximal inhibitory concentration; TCGA, The Cancer Genome Atlas.

Techniques: Expressing, Western Blot, Knockdown, CCK-8 Assay, Cell Counting, Concentration Assay

Knockdown of TERF2 suppresses AML progression and enhances cuproptosis sensitivity in vivo . (A,B) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted NSG mice (A) and the quantification of luciferase signals for all mice per group (B). (C) Kaplan-Meier analysis of survival of MOLM13-engrafted mice, log rank test. (D,E) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted mice treated with elesclomol (D) and the quantification of luciferase signals for all mice per group (E). (F) Kaplan-Meier analysis of survival of MOLM13-engrafted mice treated with elesclomol, log rank test. **, P<0.01. AML, acute myeloid leukemia; NSG, NOD-SCID IL2rg.

Journal: Translational Cancer Research

Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

doi: 10.21037/tcr-2025-1226

Figure Lengend Snippet: Knockdown of TERF2 suppresses AML progression and enhances cuproptosis sensitivity in vivo . (A,B) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted NSG mice (A) and the quantification of luciferase signals for all mice per group (B). (C) Kaplan-Meier analysis of survival of MOLM13-engrafted mice, log rank test. (D,E) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted mice treated with elesclomol (D) and the quantification of luciferase signals for all mice per group (E). (F) Kaplan-Meier analysis of survival of MOLM13-engrafted mice treated with elesclomol, log rank test. **, P<0.01. AML, acute myeloid leukemia; NSG, NOD-SCID IL2rg.

Techniques: Knockdown, In Vivo, Imaging, Luciferase

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rabbit anti trf2 (Novus Biologicals)

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