Ask about this productRelated genes to: TBC1D25 antibody
- Gene:
- TBC1D25 NIH gene
- Name:
- TBC1 domain family member 25
- Previous symbol:
- OATL1
- Synonyms:
- -
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-06
- Date modifiied:
- 2015-11-18
Related products to: TBC1D25 antibody
Related articles to: TBC1D25 antibody
- Influenza A virus (IAV) remains a major global health threat. Its M2 protein plays crucial roles in viral fusion, transportation, assembly, and release. Recent studies have shown that IAV impairs host autophagy flux to enhance viral replication. However, the precise mechanisms by which IAV M2 manipulates host cellular autophagy during virus replication remain unclear. In this study, we analysed cellular transcriptional responses of cells to IAV M2 overexpression and identified RAB GTPase protein RAB33B as a key factor. RAB33B was significantly up-regulated by IAV M2 and promoted IAV replication by enhancing autophagy. We further found that autophagy regulates the interaction of IAV M2, RAB33B, and LC3, facilitating M2 membrane trafficking through autophagic-like vesicles. In addition, ATG16L1 (an effector of RAB33B) and TBC1D25 (a GTPase-activating protein for RAB33B) contributed to IAV M2-induced autophagy, thereby affecting viral replication. Collectively, our findings reveal a novel mechanism in which RAB33B is essential for IAV M2 trafficking to the plasma membrane, facilitating viral replication through enhanced autophagy. These insights shed new light on the autophagy-based cellular transport mechanisms of IAV M2 and highlight potential antiviral targets. - Source: PubMed
Publication date: 2025/07/01
Ye ShaotangWang ZhenLu GangChen AoleiXu LiangLiu YongboMao JianweiWang JingyuLou GaomingXie QingmeiJia KunLi Shoujun - TBC1 domain family member 25 (TBC1D25) is a crucial mediator of signal transduction involved in the development of several diseases. Particularly, a cardioprotective role of TBC1D25 has been raised due to its antagonistic action on cardiac hypertrophy. However, whether TBC1D25 protects the myocardium from ischemia-reperfusion injury has not been reported. This work aimed to determine the role of TBC1D25 in myocardial ischemia-reperfusion (MIR) injury and to explore the potential mechanisms involved. Marked decreases in TBC1D25 levels occurred in cardiomyocytes suffering hypoxia/reoxygenation (H/R) injury in vitro and myocardium tissues of rats with MIR injury in vivo. Cardiomyocytes overexpressing TBC1D25 were protected from apoptosis and inflammation triggered by H/R, whereas TBC1D25-deficient cardiomyocytes were more sensitive to H/R injury. Intramyocardial injection of recombinant adenovirus expressing TBC1D25 into rats reduced infarct size and cardiac injury triggered by MIR injury accompanied by decreased myocardial apoptosis and inflammation. A subsequent mechanistic investigation revealed that the signaling cascade of transforming growth factor-β-activated kinase 1 (TAK1)-c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) activated under H/R or MIR conditions was markedly restrained by TBC1D25 overexpression. Moreover, TAK1 blockade remarkably reversed the TBC1D25 deficiency-induced aggravating effect on H/R injury. The work concludes that TBC1D25 protects against MIR injury through action on the TAK1-JNK/p38 MAPK signaling cascade. This work suggests TBC1D25 as a potential therapeutic target for MIR injury. - Source: PubMed
Publication date: 2023/12/15
Liu ZiwenShang FujunLi NaDong Wenting - Nonalcoholic fatty liver disease (NAFLD) is a strong stimulant of cardiovascular diseases, affecting one-quarter of the world's population. TBC1 domain family member 25 (TBC1D25) regulates the development of myocardial hypertrophy and cerebral ischemia-reperfusion injury; however, its effect on NAFLD/nonalcoholic steatohepatitis (NASH) has not been reported. In this study, we demonstrated that TBC1D25 expression is upregulated in NASH. TBC1D25 deficiency aggravated hepatic steatosis, inflammation, and fibrosis in NASH. In vitro tests revealed that TBC1D25 overexpression restrained NASH responses. Subsequent mechanistic validation experiments demonstrated that TBC1D25 interfered with NASH progression by inhibiting abnormal lipid accumulation and inflammation. TBC1D25 deficiency significantly promoted NASH occurrence and development. Therefore, TBC1D25 may potentially be used as a clinical therapeutic target for NASH treatment. - Source: PubMed
Publication date: 2023/01/30
Wu AndingYe MaoMa TengfeiShe ZhigangLi RuyanShi HongjieYang LingYi MaolinLi Huoping - TBC1Domain Family Member 25 (TBC1D25) is a protein that contains a TBC/RAB-GTPase activating protein (GAP) domain, which was shown to participate in autophagy in previous studies. However, the role of TBC1D25 in cerebral ischemia-reperfusion (I/R) injury remains unknown. In this study, we found that the mRNA and protein expression levels of TBC1D25 decreased in mouse brain after I/R injury and primary cortical neurons treated with oxygen and glucose deprivation/reoxygenation (OGD/R). Then TBC1D25 knockout (KO) mice were applied to demonstrate that TBC1D25 ablation aggravated cerebral I/R-induced neuronal loss and infarct size. In addition, neuronal apoptosis and inflammation were significantly potentiated in the TBC1D25-KO group. In in vitro OGD/R model, TBC1D25 knockdown can attenuate neuronal cell viability and aggravate the process of inflammation and apoptosis. Conversely, over-expression of TBC1D25 in primary neurons ameliorated the aforementioned processes. Mechanistically, RNA-sequencing (RNA-seq) analysis revealed mitogen-activated protein kinase (MAPK) signaling pathway was the most significant pathway that contributed to TBC1D25-mediated brain I/R injury process. Through experimental verification, TBC1D25 deficiency increased the phosphorylation of the transforming growth factor-β-activated kinase 1 (TAK1)-c-Jun N-terminal kinase (JNK)/p38 axis in neurons during the brain I/R injury. Furthermore, we found that TAK1 blockade abrogated the apoptosis and inflammatory response produced by TBC1D25 knockdown in vitro. In conclusion, this study is the first to demonstrate the functional significance of TBC1D25 in the pathophysiology of brain I/R injury, and the protective mechanism of TBC1D25 is dependent on the TAK1-JNK/p38 pathway. - Source: PubMed
Publication date: 2021/12/12
Zhang ZongyongMa TengfeiFu ZhengyiFeng YuWang ZhenTian SongLiu ZhenWei WeiLi XiangChen JincaoZhao Wenyuan - Male infertility is a heterogeneous disorder which may result from disruption in molecular and cellular pathways involved in spermatogenesis. Several reports have described abnormal spermatogenesis because of defective autophagy in model organisms. In the present study, we have clinically and genetically characterized a family segregating oligozoospermia in X-linked pattern. Exome sequencing revealed a disease-causing missense variant [NM_002536, c.149 A > C, p.(Glu50Ala)] in TBC1D25, an autophagy gene located on human chromosome Xp11.23. In view of broad expression of the gene in testes and effect of the variant on its interaction with ATG8 homologues, we consider a possible role for the TBC1D25 variant in causing oligozoospermia in the present family. This is the first report describing the involvement of TBC1D25 in causing male infertility. - Source: PubMed
Publication date: 2021/01/15
Nawaz ShoaibHussain ShabirBasit SulmanAhmad Wasim