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Last update 08 May 2025

TAF1B

Last update 08 May 2025

Basic Info

Synonyms

RAF1B, RAFI63, RNA polymerase I-specific TBP-associated factor 63 kDa

+ [8]

Introduction

Component of RNA polymerase I core factor complex that acts as a GTF2B/TFIIB-like factor and plays a key role in multiple steps during transcription initiation such as pre-initiation complex (PIC) assembly and postpolymerase recruitment events in polymerase I (Pol I) transcription. Binds rDNA promoters and plays a role in Pol I recruitment as a component of the SL1/TIF-IB complex and, possibly, directly through its interaction with RRN3.

Drugs associated with TAF1B

FMPV-3

Target

ASTE1 x TAF1B x TGFBR2

Mechanism

ASTE1 modulators [+2]

Active Org.

Hubro Therapeutics AS

Originator Org.

Hubro Therapeutics AS

Active Indication

Hereditary Nonpolyposis Colorectal Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TAF1B

100 Translational Medicine associated with TAF1B

0 Patents (Medical) associated with TAF1B

Literatures (Medical) associated with TAF1B

01 Jan 2024·Heliyon

Inhibition of TAF1B impairs ribosome biosynthesis and suppresses cell proliferation in stomach adenocarcinoma through promoting c-MYC mRNA degradation

Article

Author: Zhu, Sheng-Mei ; Zhang, Feng ; Liu, Ming ; Yu, Chun ; Peng, Zheng ; Yan, Jing-Yi ; Wu, Qi ; Xu, Li-Feng ; Bai, Yong-Feng ; Li, Zhang-Ping ; Qian, Mao-Xiang ; Chen, Hang-Fei

Hyperactivation of ribosome biosynthesis (RiBi) is a hallmark of cancer, and targeting ribosome biogenesis has emerged as a potential therapeutic strategy. The depletion of TAF1B, a major component of selectivity factor 1 (SL1), disrupts the pre-initiation complex, preventing RNA polymerase I from binding ribosomal DNA and inhibiting the hyperactivation of RiBi. Here, we investigate the role of TAF1B, in regulating RiBi and proliferation in stomach adenocarcinoma (STAD). We disclosed that the overexpression of TAF1B correlates with poor prognosis in STAD, and found that knocking down TAF1B effectively inhibits STAD cell proliferation and survival in vitro and in vivo. TAF1B knockdown may also induce nucleolar stress, and promote c-MYC degradation in STAD cells. Furthermore, we demonstrate that TAF1B depletion impairs rRNA gene transcription and processing, leading to reduced ribosome biogenesis. Collectively, our findings suggest that TAF1B may serve as a potential therapeutic target for STAD and highlight the importance of RiBi in cancer progression.

19 May 2023·Children (Basel, Switzerland)

Whole Exome-Trio Analysis Reveals Rare Variants Associated with Congenital Pouch Colon.

Article

Author: Suravajhala, Prashanth ; Medicherla, Krishna Mohan ; Bandapalli, Obul Reddy ; Mishra, Ashwani Kumar ; Mathur, Praveen ; Gupta, Sonal

Anorectal malformations (ARM) are individually common, but Congenital Pouch Colon (CPC) is a rare anorectal anomaly that causes a dilated pouch and communication with the genitourinary tract. In this work, we attempted to identify de novo heterozygous missense variants, and further discovered variants of unknown significance (VUS) which could provide insights into CPC manifestation. From whole exome sequencing (WES) performed earlier, the trio exomes were analyzed from those who were admitted to J.K. Lon Hospital, SMS Medical College, Jaipur, India, between 2011 and 2017. The proband exomes were compared with the unaffected sibling/family members, and we sought to ask whether any variants of significant interest were associated with the CPC manifestation. The WES data from a total of 64 samples including 16 affected neonates (11 male and 5 female) with their parents and unaffected siblings were used for the study. We examined the role of rare allelic variation associated with CPC in a 16 proband/parent trio family, comparing the mutations to those of their unaffected parents/siblings. We also performed RNA-Seq as a pilot to find whether or not the genes harboring these mutations were differentially expressed. Our study revealed extremely rare variants, viz., TAF1B, MUC5B and FRG1, which were further validated for disease-causing mutations associated with CPC, further closing the gaps of surgery by bringing intervention in therapies.

01 Jan 2023·Frontiers in oncology

TAF1B depletion leads to apoptotic cell death by inducing nucleolar stress and activating p53-miR-101 circuit in hepatocellular carcinoma.

Article

Author: Jiang, Xin-Qing ; Fang, Jian ; Xu, Li-Feng ; Xu, Heng ; Sheng, Hao ; Chen, Hang-Fei ; Zheng, Quan ; Qian, Mao-Xiang ; Yuan, Lei ; Liu, Ming ; Wu, Qi ; Zhai, Qiao-Cheng ; Zhang, Feng ; Gao, Dan-Dan

BackgroundTAF1B (TATA Box Binding Protein (TBP)-Associated Factor) is an RNA polymerase regulating rDNA activity, stress response, and cell cycle. However, the function of TAF1B in the progression of hepatocellular carcinoma (HCC) is unknown.ObjectiveIn this study, we intended to characterize the crucial role and molecular mechanisms of TAF1B in modulating nucleolar stress in HCC.MethodsWe analyzed the differential expression and prognostic value of TAF1B in hepatocellular carcinoma based on The Cancer Genome Atlas (TCGA) database, tumor and paraneoplastic tissue samples from clinical hepatocellular carcinoma patients, and typical hepatocellular carcinoma. We detected cell proliferation and apoptosis by lentiviral knockdown of TAF1B expression levels in HepG2 and SMMC-7721 cells using clone formation, apoptosis, and Western blotting (WB) detection of apoptosis marker proteins. Simultaneously, we investigated the influence of TAF1B knockdown on the function of the pre-initiation complex (PIC) by WB, and co-immunoprecipitation (Co-IP) and chromatin immunoprecipitation (ChIP) assays verified the interaction between the complexes and the effect on rDNA activity. Immunofluorescence assays measured the expression of marker proteins of nucleolus stress, fluorescence in situ hybridization (FISH) assays checked the rDNA activity, and qRT-PCR assays tested the pre-rRNA levels. Regarding molecular mechanisms, we investigated the role of p53 and miR-101 in modulating nucleolar stress and apoptosis. Finally, the impact of TAF1B knockdown on tumor growth, apoptosis, and p53 expression was observed in xenograft tumors.ResultWe identified that TAF1B was highly expressed in hepatocellular carcinoma and associated with poor prognosis in HCC patients. TAF1B depletion modulated nucleolar stress and apoptosis in hepatocellular carcinoma cells through positive and negative feedback from p53-miR-101. RNA polymerase I transcription repression triggered post-transcriptional activation of miR-101 in a p53-dependent manner. In turn, miR-101 negatively feeds back through direct inhibition of the p53-mediated PARP pathway.ConclusionThese findings broaden our comprehension of the function of TAF1B-mediated nucleolar stress in hepatocellular carcinoma and may offer new biomarkers for exploring prospective therapeutic targets in HCC.

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TAF1B

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