ATP6V1F
- Known as:
- ATP6V1F
- Catalog number:
- 002239A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATP6V1F
Related genes to: ATP6V1F
- Gene:
- ATP6V1F NIH gene
- Name:
- ATPase H+ transporting V1 subunit F
- Previous symbol:
- -
- Synonyms:
- ATP6S14, VATF, Vma7
- Chromosome:
- 7q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-09
- Date modifiied:
- 2016-02-11
Related products to: ATP6V1F
anti-ATP6V1Fanti-ATP6V1Fanti-ATP6V1F type: Primary antibodies host: MouseATP6S14,ATP6V1F,Bos taurus,Bovine,Vacuolar proton pump subunit F,VATF,V-ATPase 14 kDa subunit,V-ATPase subunit F,V-type proton ATPase subunit FATP6S14,ATP6V1F,Homo sapiens,Human,Vacuolar proton pump subunit F,VATF,V-ATPase 14 kDa subunit,V-ATPase subunit F,V-type proton ATPase subunit FAtp6s14,Atp6v1f,Mouse,Mus musculus,Vacuolar proton pump subunit F,Vatf,V-ATPase 14 kDa subunit,V-ATPase subunit F,V-type proton ATPase subunit FAtp6s14,Atp6v1f,Rat,Rattus norvegicus,Vacuolar proton pump subunit F,Vatf,V-ATPase 14 kDa subunit,V-ATPase subunit F,V-type proton ATPase subunit FATP6V1E1 Gene ATPase, H+ transporting, lysosomal 31kDa, V1 subunit E1ATP6V1F antibody Host rabbitATP6V1F antibody Host MouseATP6V1F antigenATP6V1F antigenATP6V1F antigenATP6V1F antigenATP6V1F (Human) Recombinant Protein (P01) Related articles to: ATP6V1F
- Cerebral small vessel disease (CSVD) is a major contributor to vascular dementia. Given the absence of effective treatments, the development of blood-based biomarkers for early diagnosis and prediction is paramount to facilitate targeted clinical interventions. We aimed to identified blood-based extracellular vesicle (EV) biomarkers for screening CSVD with normal cognition (CSVD-NC) or cognitive impairment (CSVD-CI), and predicting disease progression. - Source: PubMed
Publication date: 2026/05/14
Yang DanLiu PinyiHan MengxiKe ZhihongTan YiYu LinjieHu ZheqiMao ChengluCheng YueZhang HaoZhang YunZhu XiaoleiXu Yun - Colorectal cancer (CRC) stands as a significant contributor to cancer-related mortality. Owing to its prognostic and therapeutic implications, intratumoural heterogeneity (ITH) presents a considerable challenge. We have developed an experimental framework integrating single-cell derived spheroids with proteomic profiling to facilitate a molecular, proteomic, and therapeutic characterization of intratumoural heterogeneity during CRC progression. - Source: PubMed
Publication date: 2026/01/24
Radloff Helene SophiaKohl MichaelSauer ThorbenHartwig SonjaGeisler SvenLehr StefanGemoll Timo - Immune checkpoint inhibitors (ICIs) have revolutionized cancer immunotherapy, but many patients develop resistance. While the immunosuppressive effects of ultraviolet (UV) light are well-documented, its link to ICI resistance remains unclear. - Source: PubMed
Publication date: 2025/09/26
Zhang DanHuaDai MeiYing JiaFeiHuang YiFanLiu ZiXuanWu ChenLu - Macrophages play a critical role in carotid plaque. Understanding the mechanisms of carotid plaque formation based on macrophage heterogeneity could provide valuable insights for clinical intervention. Single-cell transcriptome and bulk RNA-seq data of carotid plaque were obtained from public databases. Weighted gene correlation network analysis (WGCNA) identified gene modules linked to unstable plaques. Macrophage marker genes were intersected with module genes of WGCNA, followed by using randomForest and LASSO regression to pinpoint key genes. Quantitative real-time PCR (qRT-PCR) and Western blot were used to verify the regulation of key genes at the cellular level. The correlation between the key genes and inflammatory phenotypes was examined by single-sample gene set enrichment analysis (ssGSEA). Single-cell clustering revealed major cellular subpopulations, with elevated macrophage infiltration in carotid plaque. Six key macrophage-associated genes (, and ) were discovered. The qRT-PCR results demonstrated upregulation of , and genes in vascular smooth muscle cells (VSMCs) treated with oxidized low-density lipoprotein (ox-LDL), except for , which was downregulated. Protein expression results showed that expressions of , and were significantly elevated in the ox-LDL-VSMC group. In addition, most of the immune cells showed significant differences between the unstable arterial plaque group and the control group. This study discovered potential biomarkers that affected carotid plaque progression and macrophage regulation at the single-cell level, and examined their regulatory roles in immune regulation, programed cell death (PCD), and inflammatory factor modulation. - Source: PubMed
Publication date: 2025/07/21
Ding YakunNiu XiaoyangGuo PengWang Bing - Autophagy plays a critical role in colitis-associated colorectal cancer (CAC). However, non-autonomous regulation of macroautophagic/autophagic flux during inflammation remains largely unexplored. Here, we show that deficiency ([ΔIEC]) aggravated azoxymethane-dextran sulfate sodium-induced CAC based on tumor number and burden, promoted autophagy dysfunction characterized by SQSTM1/p62 accumulation and autophagosome-lysosome fusion inhibition in IECs, and reduced lysosomal acidification by suppressing FOXA2-induced V-ATPase transcription. or overexpression rescued autophagy impairment, reactive oxygen species accumulation, and DNA damage induced by deficiency and . Neutrophil-derived serine proteases suppressed expression, causing autophagy dysfunction. knockout completely blocked the effects of neutrophil proteases on and . The correlation between neutrophil and activities was validated in ulcerative colitis and colorectal carcinoma. Therefore, deficiency in intestinal epithelial cells suppressed expression, leading to V-ATPase-mediated autophagic dysfunction and exacerbating CAC. Neutrophils may contribute to impaired autophagy and promote CAC by inactivating canonical F2RL1/PAR2 signaling via its derived proteases. F2RL1/PAR2 signaling may participate in maintaining intestinal homeostasis via autophagy. These findings provide useful insights into F2RL1/PAR2 and its cleaving serine proteases in CAC and would help in developing new therapeutic strategies for this malignancy.: AOM: azoxymethane; ATP6V0C: ATPase H+ transporting V0 subunit c; ATP6V0E1: ATPase H+ transporting V0 subunit e1; ATP6V1C2: ATPase H+ transporting V1 subunit C2; ATP6V1F: ATPase H+ transporting V1 subunit F; CAC: colitis-associated colorectal cancer; CRC: colorectal cancer; CTSB: cathepsin B; CTSG: cathepsin G; DEGs: differentially expressed genes; DSS: dextran sulfate sodium; FOXA2: forkhead box protein A2; F2RL1: F2R like trypsin receptor 1; IBD: inflammatory bowel disease; IECs: intestinal epithelial cells; LAMP1: lysosomal associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; ROS: reactive oxygen species; SQSTM1/p62: sequestosome 1; TFs: transcription factors; UC: ulcerative colitis. - Source: PubMed
Publication date: 2025/04/17
Yuan JunhuMa JianhuiZhang FanyuWang TanJian XiaxiangWang BingzhiLi WeiweiZhang XiaoliCao YubinYang HongMa YimingWang Hongying