Ask about this productRelated genes to: VPS37A Blocking Peptide
- Gene:
- VPS37A NIH gene
- Name:
- VPS37A subunit of ESCRT-I
- Previous symbol:
- PQBP2
- Synonyms:
- FLJ32642, HCRP1, SPG53
- Chromosome:
- 8p22
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-08
- Date modifiied:
- 2019-01-31
Related products to: VPS37A Blocking Peptide
Related articles to: VPS37A Blocking Peptide
- In order to investigate the basic genetic structure of plumage colour in Jingyuan chicken and to explore the genetic markers for plumage colour development, the present study was carried out to investigate the candidate key SNPs and candidate genes regulating black, linen and white plumage and plumage traits of Jingyuan chicken by using selection signal analysis and genome-wide association analysis. Selection signal analyses showed that including 30, 40 and 18 overlapping genes were associated with black, linen and white plumage colours in Jingyuan chicken. Meanwhile, integrative genomic analyses identified BCAT1, LMO3, and PIK3C2G as primary candidates for black plumage, and IL1RAPL1 for white plumage, with all genes showing convergent support across multiple complementary approaches. Further screening through Fst and θπ values identified 10 key candidate genes significantly associated with plumage colour traits, including ARFGEF2, VPS37A, SNX12, KIT, MET, ROS1, CSF1R, NGF, CDC42, and TEK. These results provide a fundamental theoretical basis for the genetic structure and formation of Jingyuan chicken plumage. - Source: PubMed
Publication date: 2025/08/06
Yang LijuanZhao WeiChen SiyuXue LinTian JinliXu HairongZhang HaiboWang HuaGu YalingZhang Juan - VPS37A (VPS37A subunit of ESCRT-I), a component of the ESCRT-I (endosomal sorting complex required for transport I) complex, mediates vesicular trafficking through sorting endocytic ubiquitinated cargos into multivesicular bodies (MVBs). Although accumulating evidence indicates that VPS37A deficiency occurs in numerous malignancies and exerts tumor-suppressive effects during cancer progression, its functional significance in colorectal cancer (CRC) pathogenesis remains poorly characterized. Therefore, this study aims to further investigate the functional and molecular mechanisms by which VPS37A downregulation contributes to malignant biological phenotypes in CRC, with a specific focus on how its dysregulation affects cell death pathways. - Source: PubMed
Publication date: 2025/07/18
Liu ChunchengLiu XiaohanLi ZiqiWei YanruoxueLiu BangdongZhu PengLiu YukunZhao Ran - Inflammation has been related to major depressive disorder pathophysiology. Autophagy, a degradative pathway regulating inflammation and immunity, has emerged as a potential contributor. Among others, we characterized, in frontal cortex (FC) and hippocampus (Hp), autophagy markers (upregulations in mTOR, ATG7, and ATG 16L1, and downregulations in ULK1, BECLIN1, phospho-SQSTM1, ATG3, ATG12, and ATG 16L1), effectors of the endosomal sorting complexes required for transport (overexpression in HRS, VPS37A, CHMP6, and GALECTIN 3, and downregulations in STAM2, TSG101, VPS28, VPS37A, CHMP5, VPS4B, and GALECTIN 9), and lysosomal proteins (LAMP1, LAMP2A, MANNOSE RECEPTOR, HSC70, HSP70, CATHEPSIN D and B, and CYSTATIN C, whose variations are dependent on lysosomal nature and brain region) of male rats exposed to chronic mild stress, a model of depression, compared to control rats. Results indicate that chronic stress alters protein expression of autophagy and the endosomal sorting complexes required for transport markers in a region-specific manner, plus increases lysosomal presence, oppositely modulating lysosomal proteins in each structure. Additionally, astrocytes seemed to exert an essential role in the regulation of the autophagy adaptor SQSTM1/p62. In conclusion, stress-induced protein disruptions in these pathways highlight their differential modulation after chronic stress exposure and their potential role in maintaining brain homeostasis during the stress response, making them promising targets for new therapeutic strategies in stress-related pathologies. - Source: PubMed
Publication date: 2025/03/07
Ulecia-Morón CristinaBris Álvaro GMacDowell Karina SCerveró-García PilarMadrigal José L MGarcía-Bueno BorjaPereira Marta PLeza Juan CCaso Javier R - Mortality from colorectal cancer (CRC) is significant, and novel CRC therapies are needed. A pseudokinase MLKL typically executes necroptotic cell death, and MLKL inactivation protects cells from such death. However, we found unexpectedly that MLKL gene knockout enhanced CRC cell death caused by a protein synthesis inhibitor homoharringtonine used for chronic myeloid leukemia treatment. In an effort to explain this finding, we observed that MLKL gene knockout reduces the basal CRC cell autophagy and renders such autophagy critically dependent on the presence of VPS37A, a component of the ESCRT-I complex. We further found that the reason why homoharringtonine enhances CRC cell death caused by MLKL gene knockout is that homoharringtonine activates p38 MAP kinase and thereby prevents VPS37A from supporting autophagy in MLKL-deficient cells. We observed that the resulting inhibition of the basal autophagy in CRC cells triggers their parthanatos, a cell death type driven by poly(ADP-ribose) polymerase hyperactivation. Finally, we discovered that a pharmacological MLKL inhibitor necrosulfonamide strongly cooperates with homoharringtonine in suppressing CRC cell tumorigenicity in mice. Thus, while MLKL promotes cell death during necroptosis, MLKL supports the basal autophagy in CRC cells and thereby protects them from death. MLKL inactivation reduces such autophagy and renders the cells sensitive to autophagy inhibitors, such as homoharringtonine. Hence, MLKL inhibition creates a therapeutic vulnerability that could be utilized for CRC treatment. - Source: PubMed
Publication date: 2025/02/20
Jiang PeijiaChipurupalli SandhyaYoo Byong HoonLiu XiaoyangRosen Kirill V - The endosomal sorting complex required for transport (ESCRT) machinery is a membrane abscission system that mediates various intracellular membrane remodeling processes, including macroautophagy/autophagy. In our recent study, we established the unique requirement of the ubiquitin E2 variant-like (UEVL) domain of the ESCRT-I subunit VPS37A for phagophore closure, the final step in autophagosome biogenesis, and determined the physiological impact of systemically inhibiting closure by targeting this region in mice. While the mutant mice exhibited phenotypes similar to those reported in mice deficient in generating ATG8 (mammalian Atg8 homologs)-conjugated (ATG8ylated) phagophores, certain phenotypes, such as neonatal lethality and liver injury, were found to be notably milder. Further investigation revealed that ATG8ylated phagophores promote TBK1-dependent SQSTM1 phosphorylation and droplet formation, leading to the formation of large insoluble aggregates upon closure inhibition. These findings suggest potential roles for ATG8ylated membranes in mitigating proteotoxicity by efficiently concentrating and sequestering soluble, reactive microaggregates and converting them into less reactive, insoluble large aggregates. The study highlights VPS37A UEVL mutant mice as a model for investigating the physiological and pathological roles of phagophores that extend beyond degradation. - Source: PubMed
Publication date: 2025/02/24
Hamamoto KoutaLiang XinwenOpozda David MWang Hong-GangTakahashi Yoshinori