YWHAB

Last update 08 May 2025

Basic Info

Synonyms

14-3-3 protein beta/alpha, 14-3-3 protein beta/alpha, N-terminally processed, KCIP-1

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Introduction

Adapter protein implicated in the regulation of a large spectrum of both general and specialized signaling pathways. Binds to a large number of partners, usually by recognition of a phosphoserine or phosphothreonine motif. Binding generally results in the modulation of the activity of the binding partner. Negative regulator of osteogenesis. Blocks the nuclear translocation of the phosphorylated form (by AKT1) of SRPK2 and antagonizes its stimulatory effect on cyclin D1 expression resulting in blockage of neuronal apoptosis elicited by SRPK2. Negative regulator of signaling cascades that mediate activation of MAP kinases via AKAP13.

100 Clinical Results associated with YWHAB

100 Translational Medicine associated with YWHAB

0 Patents (Medical) associated with YWHAB

112

Literatures (Medical) associated with YWHAB

01 May 2025·International Journal of Biological Macromolecules

Single-cell sequencing exposes mast cell-derived CD52's anti-tumor action in breast cancer through the IL-6/JAK/STAT3 axis

Article

Author: Peng, Zexi ; Jia, Yueran ; Ji, Dangyang ; Xu, Binghe ; Lan, Bo ; Fan, Ying ; Guan, Ying ; Han, Yuhang ; Tian, Xinzhu

The aggressive nature and rapid progression of triple-negative breast cancer (TNBC), coupled with a high likelihood of recurrence and mortality, underscore the critical need for effective treatments. While immunotherapy presents promising advantages for those with triple-negative breast cancer (TNBC), its efficacy is not universal. This disparity highlights the importance of investigating survival outcomes and prognostic factors for those TNBC patients who don't respond well to immunotherapy. Our study leverages both bulk and single-cell RNA sequencing data to conduct an in-depth analysis, revealing that genes associated with mast cells (PCMT1, VDAC1, YWHAB, BRD4, BTG1, and CD52) are pivotal in prognostication for TNBC patients. Laboratory experiments have further substantiated our findings, demonstrating that the overexpression of CD52 in mast cells impedes the proliferation, invasion, and metastasis of breast cancer cells. Further anti-CD52 treatment inhibiting breast tumor growth in vivo. Additionally, we have discovered that CD52 elicits its antitumor effects by meditating the IL-6/JAK/STAT3 signaling pathway. These insights not only enhance the prognostic significance of mast cells in TNBC but also pave the way for the development of novel targeted immunotherapy strategies.

01 Jan 2025·Human Genetics

Integrative analysis of transcriptome and proteome wide association studies prioritized functional genes for obesity

Article

Author: Zhao, Qi-Gang ; Zhang, Lei ; Li, Kuan ; Yan, Shan-Shan ; Han, Bai-Xue ; Song, Zi-Tong ; Ma, Xin-Ling ; Bu, Fan ; Pei, Yu-Fang ; Luo, Yuan ; Xu, Qian

BACKGROUNDGenome-wide association studies have identified dozens of genomic loci for obesity. However, functional genes and their detailed genetic mechanisms underlying these loci are mainly unknown. In this study, we conducted an integrative study to prioritize plausibly functional genes by combining information from genome-, transcriptome- and proteome-wide association analyses.METHODSWe first conducted proteome-wide association analyses and transcriptome-wide association analyses for the six obesity-related traits. We then performed colocalization analysis on the identified loci shared between the proteome- and transcriptome-association analyses. Finally, we validated the identified genes with other plasma/blood reference panels. The highlighted genes were assessed for expression of other tissues, single-cell and tissue specificity, and druggability.RESULTSWe prioritized 4 high-confidence genes (FASN, ICAM1, PDCD6IP, and YWHAB) by proteome-wide association studies, transcriptome-wide association studies, and colocalization analyses, which consistently influenced the variation of obesity traits at both mRNA and protein levels. These 4 genes were successfully validated using other plasma/blood reference panels. These 4 genes shared regulatory structures in obesity-related tissues. Single-cell and tissue-specific analyses showed that FASN and ICAM1 were explicitly expressed in metabolism- and immunity-related tissues and cells. Furthermore, FASN and ICAM1 had been developed as drug targets.CONCLUSIONOur study provided novel promising protein targets for further mechanistic and therapeutic studies of obesity.

01 Dec 2024·Cellular Signalling

The deubiquitinase OTUB1 inhibits gluconeogenesis by stabilizing YWHAB

Article

Author: Zhao, Qingwen ; Chen, Qingyan ; Han, Shuang ; Zhang, Yingjuan ; Gao, Yue ; Liang, Ziwei ; Wang, Qianzhuo ; Wang, Yule ; Sun, Zhe ; Ding, Meng ; Lu, Ruilin ; Li, Bei ; Lu, Ruiling

Hepatic gluconeogenesis plays a crucial role in maintaining glucose homeostasis and serves as a potential therapeutic target for type 2 diabetes, while its underlying mechanisms are not fully understood. This study elucidates the role of the deubiquitinase OTU domain-containing ubiquitin aldehyde binding protein 1 (OTUB1) in gluconeogenesis. We found that hepatic OTUB1 expression is reduced in both db/db mice and patients with type 2 diabetes. Deletion of hepatic OTUB1 significantly elevates fasting blood glucose levels and increases the expression of key gluconeogenic genes. Conversely, overexpression of OTUB1 in hepatocytes mitigates diabetic hyperglycemia and enhances insulin sensitivity. It is known that the tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein β (YWHAB) functions as an inhibitor of hepatic gluconeogenesis by interacting with forkhead box protein O (FOXO1) and glucagon receptor (GPCR), but its own modification mechanism remains unclear. Our findings indicate that OTUB1 interacts with YWHAB and deubiquitinates it through a catalytic process, which in turn suppresses gluconeogenesis. Therefore, OTUB1 plays a pivotal role in inhibiting hepatic gluconeogenesis, highlighting its potential as a therapeutic target for type 2 diabetes.

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YWHAB

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