FAIM2 antibody
- Known as:
- FAIM2 (anti-)
- Catalog number:
- orb100198
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- FAIM2 antibody
Ask about this productRelated genes to: FAIM2 antibody
- Gene:
- FAIM2 NIH gene
- Name:
- Fas apoptotic inhibitory molecule 2
- Previous symbol:
- -
- Synonyms:
- KIAA0950, LFG, NMP35, LIFEGUARD, TMBIM2, LFG2
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2002-10-08
- Date modifiied:
- 2016-10-05
Related products to: FAIM2 antibody
Related articles to: FAIM2 antibody
- Despite strong adaptive traits, the reproductive efficiency of Bali cattle () remains suboptimal, with low conception rates following artificial insemination (AI). Cervical mucus (CM) is a critical factor in sperm transport and fertilization; however, its molecular basis in relation to fertility has not been elucidated in this indigenous breed. This study aimed to characterize the proteomic profile of CM in Bali heifers and to identify protein biomarkers associated with fertility-related mucus quality. - Source: PubMed
Publication date: 2026/01/14
Yusuf MuhammadToleng Abdul LatiefHasrin HasrinBaharun AbdullahDiansyah Athhar ManabiSantoso SantosoRahmat RahmatAlfian Andi MuhammadMasturi MasturiSahiruddin SahiruddinAmrullah Muhammad FajarAdam Ahmad Alfaruqi SyahrandiJannah Miftahul - Lysosomal membrane proteins play fundamental roles in the lysosomal degradation of proteins and are attractive drug targets for metabolic dysfunction-associated fatty liver disease (MAFLD). Fas apoptotic inhibitory molecule 2 (FAIM2), a lysosomal membrane protein, has been recognized as an inhibitor of apoptosis in a variety of diseases. Here we reveal that FAIM2 is an inhibitor of fatty acid synthesis and suppresses MAFLD. FAIM2 protein expression is decreased in MAFLD. Moreover, FAIM2 is degraded by the E3 ubiquitin ligase NEDD4L through the catalysis of K48-linked ubiquitination. High-fat and high-cholesterol diet-induced hepatic steatosis, inflammation and fibrosis are aggravated in Faim2-knockout mice and alleviated in mice with AAV8-mediated FAIM2 overexpression. Furthermore, in hepatocytes, FAIM2 knockout increases the expression of genes related to fatty acid synthesis, while overexpressing FAIM2 exhibits the opposite effect. Mechanistically, FAIM2 directly interacts with CREB-regulated transcription coactivator 2 (CRTC2), a prominent regulator of lipid metabolism, and mediates its degradation through autophagy. Specifically, we find that the N terminus of FAIM2, which interacts with CRTC2 and LC3, is required for autophagic degradation of CRTC2. Collectively, our findings reveal that FAIM2 acts as a fatty acid synthesis inhibitor in MAFLD by promoting the autophagic degradation of CRTC2 and that FAIM2-CRTC2 may be a promising therapeutic target. - Source: PubMed
Publication date: 2025/10/07
Yu YongjieHu ShaZhang TuoShi HongjieLi DajunHuang YongpingZhang YuWang HaitaoHu YufengYu HongZhao Guang-NianZhang Peng - Multiple sclerosis (MS) is a multifaceted neurodegenerative disorder influenced by genetics and lifestyle. This systematic literature review investigates the role of six obesity-associated genes, including fat mass and obesity-associated (FTO), FAS apoptosis inhibitory molecule 2 (FAIM2), Niemann-Pick disease type C1-like 1 (NPC1), glucosamine-6-phosphate deaminase 2 (GNPDA2), melanocortin-4 receptor (MC4R), and brain-derived neurotrophic factor (BDNF) in the context of MS. - Source: PubMed
Jafari AliKhoshdooz SaraBafrani Melika ArabBakhshimoghaddam FarnushAbbasi HamidDoaei Saeid - Few pharmacogenetic studies on the use of genetic variations to predict antidepressant response in obsessive-compulsive disorder (OCD) have been published. This study expanded on the limited literature on single nucleotide polymorphisms (SNPs) across previously identified putative susceptibility genes for OCD, by incorporating known functional regulatory elements for all genes of interest. We investigated 17 SNPs in 12 genes implicated in OCD risk in 206 European ancestry OCD patients with selective serotonin reuptake inhibitor (SSRI) antidepressant response data, examining functional polymorphisms in remote regulatory regions. No association was observed between any regulatory region markers tested and drug response. We observed nominally significant associations between SNPs within the serotonin 1B receptor (5HT1B; SNP rs1778258), SLIT and NTRK-like family member 5 (SLITRK5; SNP rs10450811), and fas apoptotic inhibitory molecule 2 (FAIM2; SNP rs706795), with response to any SSRI, which did not survive multiple comparisons. This study supports a potential role for a number of OCD-associated risk genes in response to antidepressant treatment, warranting further investigation. - Source: PubMed
Publication date: 2025/03/05
Zai GwynethZai Clement CGonçalves Vanessa FWigg KarenLochner ChristineStein Dan JMathews Carol AKennedy James LRichter Margaret A - Pathological cardiac hypertrophy stands as a pivotal mechanism contributing to diverse cardiovascular diseases, ultimately leading to heart failure. Despite its clinical significance, the intricate molecular mechanisms instigating pathological cardiac hypertrophy remain inadequately understood. In this study, we aim to further reveal its complex pathogenesis by exploring the role of Fas apoptotic inhibitory molecule 2 (FAIM2) in modulating pathological cardiac hypertrophy. - Source: PubMed
Publication date: 2024/11/15
Zhong HuapingWu MinyuXie HepingChen XuLi JiayiDuan ZhishengChen HongLiu ZiyouLiao WeiChen Yijian