ATP6V1G1
- Known as:
- ATP6V1G1
- Catalog number:
- 002240A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATP6V1G1
Related genes to: ATP6V1G1
- Gene:
- ATP6V1G1 NIH gene
- Name:
- ATPase H+ transporting V1 subunit G1
- Previous symbol:
- ATP6J, ATP6G1
- Synonyms:
- ATP6GL, Vma10, ATP6G, DKFZp547P234
- Chromosome:
- 9q32
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-22
- Date modifiied:
- 2016-10-05
Related products to: ATP6V1G1
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- Targeted delivery systems offer a promising approach for selectively modulating cellular processes; yet the intracellular consequences of targeted nutrient delivery to trophoblast cells remain poorly defined. Here, we investigated a previously validated placenta-targeting peptide conjugated to liposomes encapsulating stable isotope-labelled L-arginine and L-lysine to examine cellular uptake and downstream molecular responses in a trophoblast-like cell model. Peptide-dependent uptake of fluorescently labelled liposomes was confirmed in BeWo cells, demonstrating selective internalisation compared with non-targeted controls. Encapsulation of isotope-labelled amino acids enabled direct quantification of intracellular delivery and incorporation into the cellular proteome using stable isotope labelling by amino acids in cell culture (SILAC). Quantitative proteomic analysis revealed coordinated changes in proteins associated with translation, metabolism, and nitric oxide synthase regulation following targeted liposomal uptake. Notably, V-type proton ATPase subunit G1 (ATP6V1G1) and large neutral amino acid transporter small subunit 1 (SLC7A5) showed increased incorporation of labelled amino acids and were independently validated by Western blotting. Together, these findings establish a proof-of-concept platform for targeted intracellular amino acid delivery to trophoblast-like cells and define the resulting proteomic responses. This work provides mechanistic insight into intracellular amino acid utilisation and a framework for future studies in placental cell biology. - Source: PubMed
Publication date: 2026/04/23
Mazey EmilyFlannery SarahFischer RomanKandzija NevaZhang WeiYamada YumaTokeshi ManabuJohnson ErrinAkbar NaveedBancroft JamesHannan Fadil MVatish Manu - MicroRNAs (miRNAs) are short RNAs that regulate gene expression, critical for development and disease. Residing in Argonaute (AGO) proteins, miRNAs target messenger RNAs via complementary base-pairing. Current miRNA-target databases rely on indirect data from AGO crosslinking immunoprecipitation (AGO-CLIP). In contrast, CLASH (Crosslinking, Ligation, and Sequencing of Hybrids) employs proximity ligation within AGO complexes, providing direct miRNA-target interaction evidence. Existing CLASH datasets remain limited to a few human and mouse samples. Here, we present CLASHub, which integrates CLASH-defined interactions with gene and miRNA expression data from human, mouse, Drosophila, and C. elegans, spanning 25 cell types and tissues, including 91 new CLASH datasets generated from 17 cell types/tissues. The datasets also include samples with knockout of ZSWIM8, an essential component in target-directed miRNA degradation (TDMD), providing insights into miRNA turnover mechanisms. CLASHub features a user-friendly Analyzer interface for CLASH, RNA-seq, miRNA-seq, and cumulative fraction curve analyses. Leveraging these tools, we uncover a TDMD trigger in the ATP6V1G1 3' UTR for miR-335-3p degradation, as well as multiple targets of miR-18a-5p. Thus, CLASHub is an online platform that enables cell/tissue-specific exploration of miRNA-target interactions, supporting miRNA and broader RNA biology research. The platform is publicly accessible at https://clashub.rc.ufl.edu/ . - Source: PubMed
Publication date: 2026/05/08
Li LuSheng PeikeHiers Nicholas MLi TianqiGrimme Acadia LWang YuzhiTraugot Conner MD'Agati Olivia MXie Mingyi - MicroRNAs direct downregulation of target mRNAs. Sometimes, however, this regulatory paradigm inverts, and a target RNA triggers degradation of a microRNA. This target-directed microRNA degradation (TDMD) requires ZSWIM8. mice exhibit reduced growth and perinatal lethality, accompanied by stabilization of >40 microRNAs. Nonetheless, studies of TDMD function in mammals have been limited because only two TDMD-triggering RNAs have been identified in mice. Here, we computationally identify and validate five new TDMD-triggering sites in mouse models. One site in and two sites in direct degradation of miR-335-3p, showing that in mammals, two sites in the same transcript and multiple sites in different transcripts can collaborate to destabilize a microRNA. Moreover, sites in and direct degradation of miR-322 and miR-503, respectively. Mice lacking the and sites were smaller, demonstrating that target-directed degradation of miR-322 and miR-503 promotes growth. Both miR-335-3p and are maternally imprinted, implying their participation in parental conflict, but their corresponding triggers or target microRNA partners are not imprinted. Thus, 3' UTRs can participate in parental conflict not only by regulating protein production but also by engaging TDMD to access an additional layer of regulation within a network of imprinted and biallelic genes. - Source: PubMed
Publication date: 2026/04/01
Lin Daniel HElcavage Lara EKhalizeva EkaterinaBartel David P - Circadian disruption exacerbates high-fat diet-induced metabolic disease, but whether the time-of-day exercise differentially remodels the hepatic clockwork and downstream metabolic circuits remains unclear. Male C57BL/6J mice were fed normal diet or a high-fat diet (HFD) and then underwent 8 weeks of morning or afternoon treadmill training. We evaluated glucose-lipid phenotypes and hepatic core clock proteins and conducted quantitative liver proteomics with trend-based clustering, followed by immunoblot validation. Both morning and afternoon exercise mitigated high-fat diet induced weight gain, improved glucose tolerance and insulin sensitivity, and reduced hepatic lipid accumulation relative to sedentary HFD controls, with greater benefits in the morning. HFD increased hepatic CLOCK, BMAL1, and CRY1 and suppressed REV-ERBĪ±. Morning training preferentially normalized CLOCK, BMAL1, and CRY1, whereas afternoon training more prominently restored REV-ERBĪ±. Proteomics identified two dynamic modules. Cluster 1 consists of proteins induced by diet and suppressed by exercise, including enzymes of bile acid synthesis such as CYP7A1 and components of protein N-glycosylation and endoplasmic reticulum proteostasis such as DAD1 and DPAGT1, which shifted toward control levels with exercise intervention. Cluster 7 comprises proteins reduced by diet and enhanced by exercise, including IDNK involved in nucleotide metabolism and ATP6V1G1 associated with autophagy and lysosomal function, with a stronger recovery after morning training. Immunoblotting corroborated these protein level changes. Exercise acts as a time-of-day-dependent modulator of the hepatic proteome. Morning exercise produced a more pronounced normalization of proteins implicated in bile acid metabolism, ER proteostasis, and autophagy-lysosome pathways, thereby nominating candidate mechanisms that may contribute to improved metabolic control under HFD. - Source: PubMed
Publication date: 2026/03/18
Huang ChunxiuWang XiaodanZhou HuanghaoZhu JingFangHu YueWu HuijuanYu XinruChen Cong - In avian species, the chorioallantoic membrane (CAM) is a vital, highly vascularized extraembryonic structure that supports embryonic respiration, calcium transport, and innate immune defense. In this study, we applied LC/MS/MS-based proteomics to CAM tissue harvested at embryonic days (ED) 6, 8, 10, and 12 to characterize its protein profile during the expression of different CAM functionalities during embryonic development and gain insight into possible sex-based distinctions. A total of 2688 proteins were identified, with 2347, 2265, 2351, and 1267 proteins detected at ED 6, 8, 10, and 12, respectively. Notably, 1191 common proteins were identified across all stages, while 124, 47, 86, and 2 proteins were uniquely expressed at ED 6, 8, 10, and 12, respectively. Functional annotation revealed correlations with abundant CAM protein constituents (as per their emPAI); for example: calcium mobilization - v-type proton ATPase subunit E1 (ATP6V1E1) and G1 (ATP6V1G1); intracellular transport-calcium-binding protein 39 (CAB39); vascular system and gaseous exchange - annexin A2 (ANXA2); lymphatics-actin, gamma 1 (ACTG1); blood elements-hemoglobin subunit alpha-1 (HBA1); immune defense-cathelicidin-1 (CATH1), cathelicidin-2 (CATH2); and protection against luminal toxic contents-thioredoxin (TXN). Notably, a sex-specific analysis identified 614, 320, 314, and 212 proteins that were uniquely expressed in female embryos, and 212, 273, 144, and 56 proteins only in male embryos at ED 6, 8, 10, and 12, respectively. The identification of sex-linked proteins during early CAM development may provide insight into their functional roles and highlight the CAM's potential as a target for the development of sex identification technology. - Source: PubMed
Publication date: 2025/12/24
Ali SofhianAhmed Tamer A EShrestha AgrimaHincke Maxwell T