TERF2 antibody - C-terminal region (ARP30228_T100)
- Known as:
- TERF2 (anti-) - C-terminal region (ARP30228_T100)
- Catalog number:
- arp30228_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TERF2 antibody - C-terminal region (ARP30228_T100)
Related genes to: TERF2 antibody - C-terminal region (ARP30228_T100)
- Gene:
- TERF2 NIH gene
- Name:
- telomeric repeat binding factor 2
- Previous symbol:
- TRBF2
- Synonyms:
- TRF2
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-20
- Date modifiied:
- 2016-04-25
Related products to: TERF2 antibody - C-terminal region (ARP30228_T100)
Related articles to: TERF2 antibody - C-terminal region (ARP30228_T100)
- - Source: PubMed
Publication date: 2026/04/09
Sustek SamanthaMessick Troy EDheekollu JayarajuAlbitz ColtinChen ChristopherFaustino AnnelieseTang Hsin-YaoKim Hee JongMurakami KenjiLieberman Paul M - The telomere long noncoding RNA TERRA forms R-loops in vitro at telomeres in a RAD51AP1-dependent manner. In classic DNA double-strand break repair, RAD51AP1 promotes R-loop formation and enables RAD51 to form D-loops by promoting the invasion of local RNA transcripts into donor DNA to form DNA-RNA (DR)-loops. We have previously shown that cells lacking the basic domain of TRF2 and functional RAP1 accumulate telomere D-loops, resulting in homology-directed repair (HDR)-mediated telomere-telomere clustering and formation of ultrabright telomeres (UTs). TRF2B also cooperates with RAP1 to repress telomere R-loop formation in UTs. TERRA has been shown to promote telomere HDR, associating telomeres during R-loop formation. However, the mechanism behind TERRA-mediated telomere HDR and how the TRF2-RAP1 complex regulates telomere R-loops remain unclear. Using reconstituted biochemical systems, we found that RAD51AP1 and TERRA-dependent R-loops promote RAD51-mediated telomere D-loop formation in a TERRA length- and sequence-dependent manner. Specifically, RAD51-ssDNA filaments capture telomere R-loops preferentially over dsDNA. We also discovered that BLM's interaction with the TRF2-RAP1 complex is required to promote BLM helicase-mediated unwinding of telomere R-loops. Importantly, BLM-deficient cells and cells reconstituted with BLM mutants unable to interact with TRF2 accumulate telomere R-loops in UTs. Our findings highlight a novel mechanism revealing that the TRF2-RAP1-BLM complex removes R-loops at telomeres to inhibit the generation of telomere D-loops, thus repressing telomere HDR and UT formation. - Source: PubMed
Liang FengshanChang Sandy - Establishment of sister chromatid cohesion N-acetyltransferase 2 (ESCO2) is an acetyltransferase involved in sister chromatid cohesion. Here we demonstrated that ESCO2 has a new role in telomere maintenance through its binding with telomeric repeat-binding factor TRF1 and TRF2. Loss of ESCO2 induces aberrant DNA damage at telomeres and leads to dramatic telomere shortening. ESCO2 associates with several proteins involved in DNA replication and repair, including BLM, WRN, TopBP1, BRIP1, BRCA1, and MUS81. Moreover, we show that ESCO2 acts in epistasis with BLM in promoting telomere stability. Taken together, our data suggest that ESCO2 is required for the maintenance of telomere stability, presumably by coordinating multiple replication and repair factors to facilitate telomere replication and protection. - Source: PubMed
Publication date: 2026/03/13
Guo JiahuiJi JingjingLiu JinfengTang Mengfan - Reprogramming somatic cells into induced pluripotent stem cells (iPSCs) resets the epigenetic landscapes that mark the aging clock, and consequently cells differentiated from iPSCs resemble fetal cells rather than adult or aged cells. The lack of proper cellular aging in cells differentiated from iPSCs presents a unique challenge in iPSC-based modeling of age-associated diseases such as neurodegeneration. To address this challenge, we seek to introduce cellular senescence, a hallmark of aging, into iPSC-based models in a robust and temporally controlled manner. An inducible CRISPR interference (CRISPRi) is used to suppress the expression of TERF2, a key component of the telomere protecting Shelterin complex. We demonstrate that suppression of TERF2 robustly activates the DNA damage response, p53/p21 signaling, and cellular senescence in iPSCs in a highly homogeneous and synchronous manner. Applying this inducible CRISPRi-TERF2 system to differentiation of iPSCs to neural progenitor cells (NPCs), we show efficient activation of senescence-associated phenotypes in NPCs. This inducible cell model allows isogenic comparisons of the same cell populations over the course of differentiation with or without the activation of cellular senescence in a synchronous and homogeneous manner, and has broad applications in investigating the role of cellular senescence in the progression of age-related diseases. - Source: PubMed
Neherin KashfiaHolloway KristopherSong YingduoHouston AndrewChen FengDing LiZhang Hong - Cellular senescence-related genes significantly influence the pathophysiology of ischemia–reperfusion injury (IRI). And identifying their shared biomarkers may improve the diagnosis and treatment of IRI. We analyzed three datasets (GSE61592, GSE67308, GSE83472) from the Gene Expression Omnibus database, and intersected them with the cellular senescence-related dataset to obtain 26 significantly altered cellular senescence-related differentially expressed genes in IRI. We used machine learning methods, including logistic regression, LASSO regression for feature screening, and SVM analysis, to construct a model identifying 6 key genes (, , , , , ). Internal validation shows that the model has high diagnostic accuracy. Immune infiltration analysis revealed a significant increase in 20 immune cell subpopulations in IRI. Among these, showed a strong correlation with central memory CD4 + T cells. Furthermore, regulatory network analysis revealed that is a high-priority drug target; is a hub gene regulated by transcription factors; and and are hub genes regulated by miRNAs. Finally, we validated the differential expression of these 6 genes in a mouse IRI model by qRT-PCR and immunohistochemistry. Overall, this study established a novel diagnostic model containing 6 genes. This model provides new insights into the pathological mechanisms of IRI and offers new directions for improving the early diagnosis and targeted treatment of IRI. - Source: PubMed
Publication date: 2026/01/14
Sun LianxuLiu HuanJia TingXue SongyanLi XuhaoZhang JingXing ZhizhengWang JiayiMa Jing