Polyclonal Rabbit ABHD8 Antibody
- Known as:
- Polyclonal Rabbit ABHD8 Antibody
- Catalog number:
- KA0059
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit ABHD8 Antibody
Related genes to: Polyclonal Rabbit ABHD8 Antibody
- Gene:
- ABHD8 NIH gene
- Name:
- abhydrolase domain containing 8
- Previous symbol:
- -
- Synonyms:
- FLJ11743, MGC14280, MGC2512
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-08
- Date modifiied:
- 2016-10-05
Related products to: Polyclonal Rabbit ABHD8 Antibody
Related articles to: Polyclonal Rabbit ABHD8 Antibody
- Colorectal cancer (CRC) is a highly aggressive gastrointestinal malignancy with significant global health consequences. While mitochondrial lipid metabolism genes are known to influence CRC progression, their prognostic relevance remains inadequately explored. - Source: PubMed
Publication date: 2025/11/10
Wang HouZhang KaiWang YueqiuChen MengyunZhang Mingchen - The NLRP3 inflammasome is a multiprotein complex that plays a vital role in the innate immune system in response to microbial infections and endogenous danger signals. Aberrant activation of the NLRP3 inflammasome is implicated in a spectrum of inflammatory and autoimmune diseases, emphasizing the necessity for precise regulation of the NLRP3 inflammasome to maintain immune homeostasis. The protein level of NLRP3 is a limiting step for inflammasome activation, which must be tightly controlled to avoid detrimental consequences. Here, we demonstrate that ABHD8, a member of the α/β-hydrolase domain-containing (ABHD) family, interacts with NLRP3 and promotes its degradation through the chaperone-mediated autophagy (CMA) pathway. ABHD8 acts as a scaffold to recruit palmitoyltransferase ZDHHC12 to NLRP3 for its palmitoylation as well as subsequent CMA-mediated degradation. Notably, deficiency results in the stabilization of NLRP3 protein and promotes NLRP3 inflammasome activation. We further confirm that ABHD8 overexpression ameliorates LPS- or alum-triggered NLRP3 inflammasome activation . Interestingly, the nucleocapsid (N) protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) impairs the ABHD8-NLRP3 association, resulting in an elevation in NLRP3 protein level and excessive inflammasome activation. These findings demonstrate that ABHD8 May represent a potential therapeutic target in conditions associated with NLRP3 inflammasome dysregulation. 3-MA: 3-methyladenine; ABHD: α/β-hydrolase domain-containing; BMDMs: Bone marrow-derived macrophages; CFZ: carfilzomib; CHX: cycloheximide; CMA: chaperone-mediated autophagy; CQ: chloroquine; DAMPs: danger/damage-associated molecular patterns; HSPA8/HSC70: heat shock protein family A (Hsp70) member 8; LAMP2A: lysosomal associated membrane protein 2A; NHCl: ammonium chloride; NLRP3: NLR family pyrin domain containing 3; PAMPs: pathogen-associated molecular patterns; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2. - Source: PubMed
Publication date: 2024/09/03
Yang ShuaiLi MengqiuLian GuangyuWu YaoxingCui JunWang Liqiu - Secondary progressive multiple sclerosis (SPMS) is the second most common presentation of multiple sclerosis (MS) and is characterized by a gradually deteriorating disease with or without relapses. Approximately 80% of patients with relapsing-remitting MS (RRMS) develop SPMS within 20 years. Epidemiological investigations have revealed an average 7-year life expectancy decrease (more severe in progressive subtypes) in patients with MS. Studies have focused on the neurodegenerative pathogenesis of SPMS; and epigenetic changes have been associated with disease progression in neurodegenerative disorders. However, the evidence for the association between epigenetic changes and SPMS is scarce. Thus, in this study we aimed to identify the key epigenetic genes in SPMS. - Source: PubMed
Publication date: 2022/01/07
Ye FeiDai YuanyuanWang TianzhuLiang JieWu XiaoxinLan KaiSheng Wenli - Squamous cell carcinomas (SqCC) of the aerodigestive tract have similar etiological risk factors. Although genetic risk variants for individual cancers have been identified, an agnostic, genome-wide search for shared genetic susceptibility has not been performed. To identify novel and pleotropic SqCC risk variants, we performed a meta-analysis of GWAS data on lung SqCC (LuSqCC), oro/pharyngeal SqCC (OSqCC), laryngeal SqCC (LaSqCC) and esophageal SqCC (ESqCC) cancers, totaling 13,887 cases and 61,961 controls of European ancestry. We identified one novel genome-wide significant (Pmeta<5x10-8) aerodigestive SqCC susceptibility loci in the 2q33.1 region (rs56321285, TMEM273). Additionally, three previously unknown loci reached suggestive significance (Pmeta<5x10-7): 1q32.1 (rs12133735, near MDM4), 5q31.2 (rs13181561, TMEM173) and 19p13.11 (rs61494113, ABHD8). Multiple previously identified loci for aerodigestive SqCC also showed evidence of pleiotropy in at least another SqCC site, these include: 4q23 (ADH1B), 6p21.33 (STK19), 6p21.32 (HLA-DQB1), 9p21.33 (CDKN2B-AS1) and 13q13.1(BRCA2). Gene-based association and gene set enrichment identified a set of 48 SqCC-related genes rel to DNA damage and epigenetic regulation pathways. Our study highlights the importance of cross-cancer analyses to identify pleiotropic risk loci of histology-related cancers arising at distinct anatomical sites. - Source: PubMed
Publication date: 2021/03/05
Lesseur CorinaFerreiro-Iglesias AidaMcKay James DBossé YohanJohansson MattiasGaborieau ValerieLandi Maria TeresaChristiani David CCaporaso Neil CBojesen Stig EAmos Christopher IShete SanjayLiu GeoffreyRennert GadiAlbanes DemetriusAldrich Melinda CTardon AdoninaChen ChuTriantafillos LiloglouField John KTeare Marion DawnKiemeney Lambertus ADiergaarde BrendaFerris Robert LZienolddiny ShanbehLam StephenOlshan Andrew FWeissler Mark CLacko MartinRisch AngelaBickeböller HeikeNess Andy RThomas SteveLe Marchand LoicSchabath Matthew BWünsch-Filho VictorTajara Eloiza HAndrew Angeline SClifford Gary MLazarus PhilipGrankvist KjellJohansson MikaelArnold SusanneMelander OlleBrunnström HansBoccia StefaniaCadoni GabriellaTimens WimObeidat Ma'enXiao XiangjunHoulston Richard SHung Rayjean JBrennan Paul - Osteoporosis is characterized by decreased bone mineral density and increased risk of fracture. Raloxifene is one of the treatments of osteoporosis. However, the responses were variable among patients. Previous studies revealed that the genetic variants are involved in the regulation of treatment outcomes. To date, studies that evaluate the influence of genes across all genome on the raloxifene treatment response are still limited. In this study, a total of 41 postmenopausal osteoporosis patients under regular raloxifene treatment were included. Gene-based analysis using MAGMA was applied to investigate the genetic association with the bone mineral density response to raloxifene at the lumbar spine or femoral neck site. Results from gene-based analysis indicated several genes (, , and ) related to the responses of raloxifene. Besides, the pathways of iron ion homeostasis, osteoblast differentiation, and platelet morphogenesis were enriched which implies that these pathways might be relatively susceptible to raloxifene treatment outcome. Our study provided a novel insight into the response to raloxifene. - Source: PubMed
Publication date: 2020/08/31
Lu Hsing-FangChou Po-HsinLin Gan-HongChou Wan-HsuanWang Shih-TienAdikusuma WirawanMugiyanto EkoHung Kuo-ShengChang Wei-Chiao