CHMP5
- Known as:
- CHMP5
- Catalog number:
- Y213439
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CHMP5
Related genes to: CHMP5
- Gene:
- CHMP5 NIH gene
- Name:
- charged multivesicular body protein 5
- Previous symbol:
- C9orf83, SNF7DC2
- Synonyms:
- HSPC177, CGI-34, Vps60
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-04-04
- Date modifiied:
- 2014-11-19
Related products to: CHMP5
Antibodies: CHMP5 HOST: Goat Clonality: pAbBovine Charged multivesicular body protein 5(CHMP5) ELISA kitC9orf83,CGI-34,Charged multivesicular body protein 5,CHMP5,Chromatin-modifying protein 5,Homo sapiens,HSPC177,Human,hVps60,PNAS-114,PNAS-2,SNF7 domain-containing protein 2,SNF7DC2,Vacuolar protein sorCanine Charged multivesicular body protein 5(CHMP5) ELISA kitCanine Charged multivesicular body protein 5(CHMP5) ELISA kitCharged multivesicular body protein 5,Chmp5,Chromatin-modifying protein 5,Mouse,Mus musculus,SNF7 domain-containing protein 2,Snf7dc2Charged multivesicular body protein 5,Chmp5,Chromatin-modifying protein 5,Rat,Rattus norvegicusChicken Charged multivesicular body protein 5(CHMP5) ELISA kitCHMP4B Gene chromatin modifying protein 4BCHMP5 antibody Host RabbitCHMP5 AntibodyCHMP5 (C-term) antibody Host GoatCHMP5 (C-term) antibody Ab host: GoatCHMP5 (C-term) antibody Ab host: GoatCHMP5 (C-term) Goat antibody Ab Aff - Purified Related articles to: CHMP5
- The dysfunction of the cellular endolysosomal pathway, such as in lysosomal storage diseases, can cause severe musculoskeletal disorders. However, how endolysosomal dysfunction causes musculoskeletal abnormalities remains poorly understood, limiting therapeutic options. Here, we report that CHMP5, a member of the endosomal sorting complex required for transport (ESCRT)-III protein family, is essential to maintain the endolysosomal pathway and regulate bone formation in osteogenic lineage cells. Genetic ablation of in mouse osteogenic cells increases bone formation in vivo and in vitro. Mechanistically, deletion causes endolysosomal dysfunction by decreasing the VPS4A protein, and CHMP5 overexpression is sufficient to increase the VPS4A protein. Subsequently, endolysosomal dysfunction disturbs mitochondrial functions and increases mitochondrial ROS, ultimately resulting in skeletal cell senescence. Senescent skeletal cells cause abnormal bone formation by combining cell-autonomous and paracrine actions. Importantly, the elimination of senescent cells using senolytic drugs can alleviate musculoskeletal abnormalities in conditional knockout mice. Therefore, our results show that cell senescence represents an underpinning mechanism and a therapeutic target for musculoskeletal disorders caused by the aberrant endolysosomal pathway, such as in lysosomal storage diseases. These results also uncover the function and mechanism of CHMP5 in the regulation of cell senescence by affecting the endolysosomal-mitochondrial pathway. - Source: PubMed
Publication date: 2025/07/07
Zhang FanWang YuanZhang LuyangWang ChunjieChen DepingLiu HaiboXu RenHaynes Cole MShim Jae-HyuckGe Xianpeng - Methuosis represents a novel cell death modality characterized by catastrophic cytoplasmic vacuolization in normal and malignant cells. However, the critical role and the underlying mechanism of cytoskeleton and plasma membrane damage in methuotic cells are largely unknown. - Source: PubMed
Publication date: 2025/07/05
Dong BinXiao JingWang JunqiSong XinhaoJi HuiPeng JiurongWeng XinruGuo DaweiJiang ShanxiangGao Xiuge - Addiction to oncogene-rewired transcriptional networks is a therapeutic vulnerability in cancer cells, underscoring a need to better understand mechanisms that relay oncogene signals to the transcriptional machinery. Here, using human and mouse T cell acute lymphoblastic leukemia (T-ALL) models, we identify an essential requirement for the endosomal sorting complex required for transport protein CHMP5 in T-ALL epigenetic and transcriptional programming. CHMP5 is highly expressed in T-ALL cells where it mediates recruitment of the coactivator BRD4 and the histone acetyl transferase p300 to enhancers and super-enhancers that enable transcription of T-ALL genes. Consequently, CHMP5 depletion causes severe downregulation of critical T-ALL genes, mitigates chemoresistance and impairs T-ALL initiation by oncogenic NOTCH1 in vivo. Altogether, our findings uncover a non-oncogene dependency on CHMP5 that enables T-ALL initiation and maintenance. - Source: PubMed
Publication date: 2025/05/03
Umphred-Wilson KatharineRatnayake ShashikalaTang QianziWang RuiChaudhary Sneha GhoshBallachanda Devaiah NTrichka JosephineWisniewski JanZhou LanChen QingrongMeerzaman DaoudSinger Dinah SAdoro Stanley - Outer membrane vesicles (OMVs) released by () can enter the blood circulation of the host and cause extra-gastric lesions such as atherosclerosis and hyperemesis gravidarum. This study aimed to investigate the effect of OMVs released by on the development of thymic T cells in offspring mice and its underlying mechanisms. Through experimental observations, we found that OMVs were able to cross the placental barrier, leading to a decrease in the number of CD3 and CD4 T cells in the peripheral blood of the offspring mice and a decrease in the response of T cells to stimulation. After stimulation with OMVs in T cell positive selection experiments, the expression levels of CHMP5, IKK-β, and NF-κB are up-regulated, and the release of cytokines IL-7, IL-2, IL-4, and IFN-γ is simultaneously increased, whereas in T cell negative selection experiments, the expression of JNK is up-regulated, and the expression of CHMP5 and Bcl-2 is down-regulated in E15-16 fetal thymus organ culture. These results indicate that transmission of OMVs from mother to fetus might be related to the development of central tolerance in offspring T cells. The underlying mechanism may involve an interaction between the OMVs-stimulated pathway and the TCR pathway, although further research is needed to confirm this hypothesis. The study highlights the importance of preventing infection during pregnancy and suggests that the effect of centrally tolerated antigens needs to be considered in vaccine design to maximize prevention. - Source: PubMed
Publication date: 2025/04/15
Wei YusenZhou LuZhao XiaofeiQiu HuiqingHu DailunShi Zhongli - Ferroptosis, a form of cell death discovered in recent years, is expected to provide new targets for the diagnosis and treatment of hepatocellular carcinoma (HCC) through further research. - Source: PubMed
Publication date: 2025/03/20
Li HongxuHu XinyueWang LiGu XiangranChen ShibinTang YixuanChen YuanChen JinYuan ZhengrongWang Yajie