TCEA2 antibody - N-terminal region (ARP33408_T100)
- Known as:
- TCEA2 (anti-) - N-terminal region (ARP33408_T100)
- Catalog number:
- arp33408_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TCEA2 antibody - N-terminal region (ARP33408_T100)
Related genes to: TCEA2 antibody - N-terminal region (ARP33408_T100)
- Gene:
- TCEA2 NIH gene
- Name:
- transcription elongation factor A2
- Previous symbol:
- -
- Synonyms:
- TFIIS
- Chromosome:
- 20q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-27
- Date modifiied:
- 2016-02-15
Related products to: TCEA2 antibody - N-terminal region (ARP33408_T100)
Related articles to: TCEA2 antibody - N-terminal region (ARP33408_T100)
- Epigenetic alterations during fetal development have been proposed as key factors explaining associations between maternal lifestyle during pregnancy and later health outcomes in the offspring, pertaining to the developmental origin of health and disease hypothesis. - Source: PubMed
Publication date: 2025/10/29
De Silva KushanLundberg-Ulfsdotter RichardBodén StinaVinnars Marie-ThereseRyden PatrikWest Christina EDomellöf MagnusHarlid Sophia - During DNA replication, the replisome must remove barriers and roadblocks including the transcription machinery. Transcription-replication conflicts (TRCs) occur when there are collisions between the replisome and transcription machinery, and are increasingly recognized as an important source of mammalian genome instability. How cells facilitate replisome bypass at sites of TRCs is incompletely understood. Here we show that the CUL3-KCTD10 E3 ligase senses TRCs and promotes remodelling of the RNA polymerase complex to allow replisome bypass. We found that the substrate adaptor KCTD10 interacts with the replisome and the transcription machinery and regulates both in unstressed conditions. These bivalent interactions allow KCTD10 to detect co-directional TRCs and facilitate higher-order assembly of KCTD10 complexes that recruit CUL3 to induce the ubiquitination and removal of the RNA polymerase factor TCEA2. In the absence of KCTD10, there is increased retention of TCEA2 and the RNA polymerase complex, causing an accumulation of TRCs and increased DNA damage. Our results demonstrate how replication can proceed through transcriptionally active regions, utilizing a unique bridging function of the CUL3-KCTD10 complex. These findings provide a framework for how the coordination between transcription and replication may contribute to the maintenance of genome stability. - Source: PubMed
Publication date: 2025/10/08
Kloeber Jake AChen BinSun GuangchaoKing Charles SWang ZhiquanWang LiWu ZhemingZhu ShouhaiZhao FeiQin HongranOuyang YaobinXiao HuapingTu XinyiLu JingJiang YanxiaLuo KuntianYin PingWu XinyanMutter Robert WHuang JinzhouLou Zhenkun - There is an urgent need to pinpoint novel targets for drug discovery in the context of chronic kidney disease (CKD), and the proteome represents a significant pool of potential therapeutic targets. To address this, we performed proteome-wide analyses using Mendelian randomization (MR) and colocalization techniques to uncover potential targets for CKD. We extracted summary-level data from the ARIC study, focusing on 7213 European American (EA) individuals and 4657 plasma proteins. To broaden our analysis, we incorporated genetic association data from Icelandic cohorts, thereby enhancing our investigation into the correlations with chronic kidney disease (CKD), creatinine-based estimated glomerular filtration rate (eGFRcrea), and estimated glomerular filtration rate (eGFR). We utilized genetic association data from the GWAS Catalog, including CKD (765,348, 625,219 European ancestry and 140,129 non-European ancestry), eGFRcrea (1,004,040, European ancestry), and eGFR (567,460, European ancestry). Employing MR analysis, we estimated the associations between proteins and CKD risk. Additionally, we conducted colocalization analysis to evaluate the existence of shared causal variants between the identified proteins and CKD. We detected notable correlations between levels predicted based on genetics of three circulating proteins and CKD, eGFRcrea, and eGFR. Notably, our colocalization analysis provided robust evidence supporting these associations. Specifically, genetically predicted levels of Transcription elongation factor A protein 2 (TCEA2) and Neuregulin-4 (NRG4) exhibited an inverse relationship with CKD risk, while Glucokinase regulatory protein (GCKR) showed an increased risk of CKD. Furthermore, our colocalization analysis also supported the associations of TCEA2, NRG4, and GCKR with the risk of eGFRcrea and eGFR. - Source: PubMed
Publication date: 2024/09/27
Zhao PinLi ZhenhaoXue ShilongCui JinshanZhan YonghaoZhu ZhaoweiZhang Xuepei - Chronic kidney disease (CKD) is a progressive disease for which there is no effective cure. We aimed to identify potential drug targets for CKD and kidney function by integrating plasma proteome and transcriptome. - Source: PubMed
Publication date: 2024/06/19
Si ShuchengLiu HongyanXu LuZhan Siyan - Enzalutamide, docetaxel, and cabazitaxel treatment resistance is a major problem in metastatic castration resistant prostate cancer (mCRPC), but the underlying genetic determinants are poorly understood. To identify genes that modulate treatment response to these drugs, we performed three genome-wide CRISPR/Cas9 knockout screens in the mCRPC cell line C4. The screens identified seven candidates for enzalutamide (BCL2L13, CEP135, E2F4, IP6K2, KDM6A, SMS, and XPO4), four candidates for docetaxel (DRG1, LMO7, NCOA2, and ZNF268), and nine candidates for cabazitaxel (ARHGAP11B, DRG1, FKBP5, FRYL, PRKAB1, RP2, SMPD2, TCEA2, and ZNF585B). We generated single-gene C4 knockout clones/populations for all genes and could validate effect on treatment response for five genes (IP6K2, XPO4, DRG1, PRKAB1, and RP2). Altered enzalutamide response upon IP6K2 and XPO4 knockout was associated with deregulation of AR, mTORC1, and E2F signaling, and deregulated p53 signaling (IP6K2 only) in C4 mCRPC cells. Our study highlights the necessity of performing individual validation of candidate hits from genome-wide CRISPR screens. Further studies are needed to assess the generalizability and translational potential of these findings. - Source: PubMed
Publication date: 2023/06/03
Haldrup JakobWeiss SimoneSchmidt LinnéaSørensen Karina Dalsgaard