TCERG1

Last update 08 May 2025

Basic Info

Synonyms

CA150, TAF2S, TATA box-binding protein-associated factor 2S

+ [4]

Introduction

Transcription factor that binds RNA polymerase II and inhibits the elongation of transcripts from target promoters. Regulates transcription elongation in a TATA box-dependent manner. Necessary for TAT-dependent activation of the human immunodeficiency virus type 1 (HIV-1) promoter.

100 Clinical Results associated with TCERG1

100 Translational Medicine associated with TCERG1

0 Patents (Medical) associated with TCERG1

Literatures (Medical) associated with TCERG1

01 Apr 2024·The Prostate

Whole‐exome sequencing of Nigerian benign prostatic hyperplasia reveals increased alterations in apoptotic pathways

Article

Author: Yates, Clayton ; Adeniji, Kayode A. ; Brignole, Kathryn R. ; White, Jason A. ; Ambs, Stefan ; Davis, Melissa ; Campbell, Moray J. ; Tang, Wei ; Dean‐Colomb, Windy ; Ogo, Chidiebere N. ; Obafunwa, John O. ; Jibrin, Paul ; Popoola, Ademola ; Rotimi, Solomon O. ; Odedina, Folake T. ; Fatiregun, Omolara A. ; Thorpe, Roland J. ; Kaninjing, Ernest T. ; Oluwole, Olabode P. ; Elhussin, Isra ; Karanam, Balasubramanyam ; Mohammed, Faruk ; Polak, Paz

AbstractBackgroundThrough whole‐exome sequencing of 60 formalin‐fixed paraffin‐embedded Nigerian (NGRn) benign prostatic hyperplasia (BPH) samples, we identified germline and somatic alterations in apoptotic pathways impacting BPH development and progression. Prostate enlargement is a common occurrence in male aging; however, this enlargement can lead to lower urinary tract symptoms that negatively impact quality of life. This impact is disproportionately present in men of African ancestry. BPH pathophysiology is poorly understood and studies examining non‐European populations are lacking.MethodsIn this study, NGRn BPH, normal prostate, and prostate cancer (PCa) tumor samples were sequenced and compared to characterize genetic alterations in NGRn BPH.ResultsTwo hundred and two nonbenign, ClinVar‐annotated germline variants were present in NGRn BPH samples. Six genes [BRCA1 (92%), HSD3B1 (85%), TP53 (37%), PMS2 (23%), BARD1 (20%), and BRCA2 (17%)] were altered in at least 10% of samples; however, compared to NGRn normal and tumor, the frequency of alterations in BPH samples showed no significant differences at the gene or variant level. BRCA2_rs11571831 and TP53_rs1042522 germline alterations had a statistically significant co‐occurrence interaction in BPH samples. In at least two BPH samples, 173 genes harbored somatic variants known to be clinically actionable. Three genes (COL18A1, KIF16B, and LRP1) showed a statistically significant (p < 0.05) higher frequency in BPH. NGRn BPH also had five gene pairs (PKD1/KIAA0100, PKHD1/PKD1, DNAH9/LRP1B, NWD1/DCHS2, and TCERG1/LMTK2) with statistically significant co‐occurring interactions. Two hundred and seventy‐nine genes contained novel somatic variants in NGRn BPH. Three genes (CABP1, FKBP1C, and RP11‐595B24.2) had a statistically significant (p < 0.05) higher alteration frequency in NGRn BPH and three were significantly higher in NGRn tumor (CACNA1A, DMKN, and CACNA2D2). Pairwise Fisher's exact tests showed 14 gene pairs with statistically significant (p < 0.05) interactions and four interactions approaching significance (p < 0.10). Mutational patterns in NGRn BPH were similar to COSMIC (Catalog of Somatic Mutations in Cancer) signatures associated with aging and dysfunctional DNA damage repair.ConclusionsNGRn BPH contained significant germline alteration interactions (BRCA2_rs11571831 and TP53_rs1042522) and increased somatic alteration frequencies (LMTK2, LRP1, COL18A1, CABP1, and FKBP1C) that impact apoptosis. Normal prostate development is maintained by balancing apoptotic and proliferative activity. Dysfunction in either mechanism can lead to abnormal prostate growth. This work is the first to examine genomic sequencing in NGRn BPH and provides data that fill known gaps in the understanding BPH and how it impacts men of African ancestry.

18 Nov 2022·Stem Cells Translational Medicine

Carm1 and the Epigenetic Control of Stem Cell Function

Article

Author: Rudnicki, Michael A ; Saber, John

AbstractCoactivator-associated arginine methyltransferase 1 (CARM1) is a methyltransferase whose function has been highly studied in the context of nuclear receptor signaling. However, CARM1 is known to epigenetically regulate expression of several myogenic genes involved in differentiation such as Myog and MEF2C. CARM1 also acts to regulate myogenesis through its influence on various cellular processes from embryonic to adult myogenesis. First, CARM1 has a crucial role in establishing polarity-regulated gene expression during an asymmetric satellite cell division by methylating PAX7, leading to the expression of Myf5. Second, satellite cells express the CARM1-FL and CARM1-ΔE15 isoforms. The former has been shown to promote pre-mRNA splicing through its interaction with CA150 and U1C, leading to their methylation and increased activity, while the latter displays a reduction in both metrics, thus, modulating alternative pre-mRNA splice forms in muscle cells. Third, CARM1 is a regulator of autophagy through its positive reinforcement of AMPK activity and gene expression. Autophagy already has known implications in ageing and disease, and CARM1 could follow suite. Thus, CARM1 is a central regulator of several important processes impacting muscle stem cell function and myogenesis.

01 Jun 2022·eBioMedicine

Pathophysiologic and clinical implications of molecular profiles resultant from deletion 5q

Article

Author: Barnard, John ; Haferlach, Torsten ; Arenillas, Leonor ; Meggendorfer, Manja ; Maciejewski, Jaroslaw P ; Boultwood, Jacqueline ; Adema, Vera ; Mallo, Mar ; La Framboise, Thomas ; Kern, Wolfgang ; Xicoy, Blanca ; Pellagatti, Andrea ; Visconte, Valeria ; Walter, Wencke ; Radivoyevitch, Tomas ; Hutter, Stephan ; Haferlach, Claudia ; Solé, Francesc ; Palomo, Laura ; Sekeres, Mikkael

BACKGROUNDHaploinsufficiency (HI) resulting from deletion of the long arm of chromosome 5 [del(5q)] and the accompanied loss of heterozygosity are likely key pathogenic factors in del(5q) myeloid neoplasia (MN) although the consequences of del(5q) have not been yet clarified.METHODSHere, we explored mutations, gene expression and clinical phenotypes of 388 del(5q) vs. 841 diploid cases with MN [82% myelodysplastic syndromes (MDS)].FINDINGSDel(5q) resulted as founder (better prognosis) or secondary hit (preceded by TP53 mutations). Using Bayesian prediction analyses on 57 HI marker genes we established the minimal del(5q) gene signature that distinguishes del(5q) from diploid cases. Clusters of diploid cases mimicking the del(5q) signature support the overall importance of del(5q) genes in the pathogenesis of MDS in general. Sub-clusters within del(5q) patients pointed towards the inherent intrapatient heterogeneity of HI genes.INTERPRETATIONThe underlying clonal expansion drive results from a balance between the "HI-driver" genes (e.g., CSNK1A1, CTNNA1, TCERG1) and the proapoptotic "HI-anti-drivers" (e.g., RPS14, PURA, SIL1). The residual essential clonal expansion drive allows for selection of accelerator mutations such as TP53 (denominating poor) and CSNK1A1 mutations (with a better prognosis) which overcome pro-apoptotic genes (e.g., p21, BAD, BAX), resulting in a clonal expansion. In summary, we describe the complete picture of del(5q) MN identifying the crucial genes, gene clusters and clonal hierarchy dictating the clinical course of del(5q) patients.FUNDINGTorsten Haferlach Leukemia Diagnostics Foundation. US National Institute of Health (NIH) grants R35 HL135795, R01HL123904, R01 HL118281, R01 HL128425, R01 HL132071, and a grant from Edward P. Evans Foundation.

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TCERG1

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