Ask about this productRelated genes to: ELFN2 antibody
- Gene:
- ELFN2 NIH gene
- Name:
- extracellular leucine rich repeat and fibronectin type III domain containing 2
- Previous symbol:
- LRRC62, PPP1R29
- Synonyms:
- dJ63G5.3, KIAA1904
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-10-16
- Date modifiied:
- 2016-06-06
Related products to: ELFN2 antibody
Related articles to: ELFN2 antibody
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive hepatic metabolic disorder characterized by excessive fat accumulation in hepatocytes. MASLD can advance to metabolic dysfunction-associated steatohepatitis (MASH). These conditions often lead to hepatic fibrosis, cirrhosis and hepatocellular carcinoma (HCC) if not timely diagnosed and managed; thus, molecular phenotyping of MASLD and MASH conditions is highly desirable. The analyses were performed to identify distinct, differentially expressed genes, particularly noncoding ones, in MASLD and MASH patient samples, thereby expanding diagnostic and therapeutic options. - Source: PubMed
Publication date: 2026/07/16
Delgadillo Frida MPerez KarlaYang BarbaraDhandayuthapani SubramanianYallapu Murali MChauhan Subhash CRamos Enrique IGadad Shrikanth S - is a globally prevalent foodborne zoonotic pathogen that threatens animal production and human health. Consumption of undercooked meat like pork and lamb is a major route of human infection. In this study, we performed a genome-wide CRISPR knockout screen in the porcine cell line PK15 to identify host factors that are critical for replication. The results showed that disrupting the (extracellular leucine rich repeat and fibronectin type III domain containing 2) gene in PK15 did not affect host cell growth, but significantly reduced the proliferation of parasites. Loss of decreased macroautophagy/autophagy in PK15 cells and impaired lipid metabolism, resulting in reduced lipid availability for the parasites and consequent suppression of proliferation. Exogenous lipid supplementation or pharmacological activation of autophagy could fully restore the replication of parasites in Δ cells. The requirement of host for optimal parasite proliferation was validated by constructing mice, which showed increased resistance to infection and reduced parasite burden, highlighting the value of in breeding -resistant animals. Notably, naturally occurring loss-of-function mutations in could be found in certain pig breeds, further indicating the feasibility of breeding -resistant animals like pigs, to reduce the transmission of . 3-MA: 3-methyladenine; ATG5: autophagy related 5; ATG7: autophagy related 7; BODIPY-C12: BODIPY FL C; CCK-8: Cell Counting Kit-8; ComN2: complemented with an ectopic copy of; ELFN2: extracellular leucine rich repeat and fibronectin type III domain containing 2;:homozygous knockout; FASII: type II synthesis pathway; GFP: green fluorescent protein; KO: knockout; LD: lipid droplets; MG: monoacylglycerol; MOI: multiplicity of infection; MTORC1: mechanistic target of rapamycin kinase complex 1; PV: parasitophorous vacuole; PVM: parasitophorous vacuole membrane; ; WT: wild type. - Source: PubMed
Publication date: 2026/07/01
Xu HaoLiu HailongLu TaozhenChen YukunLi YazhouZhu YuchaoWei LitingFan BolinZhang YonghuiZhang ChuangshiFang RuiXie ShengsongShen Bang - Glioblastoma (GBM) frequently develops resistance to temozolomide (TMZ), a process critically mediated by pro-survival autophagy. While phosphatase signaling plays an essential role in regulating autophagic adaptation, the specific molecular drivers that functionally link phosphatase activity to TMZ resistance through autophagy remain poorly understood. We identified ELFN2 as a brain-enriched PP1 regulatory subunit that inhibits dephosphorylation activity, leading to phosphorylation of the splicing factor SRRM1. This triggers widespread alternative splicing, particularly a proautophagic mutually exclusive exon switch in TMBIM6, thereby promoting autophagy and TMZ resistance. Upstream, the transcription factor LRRC4 represses ELFN2, while the lncRNA LINC00470 sequesters LRRC4 in the cytoplasm to antagonize this repression. Preclinically, the HDAC inhibitor Vorinostat targets ELFN2, restores PP1 activity, and synergizes with TMZ to overcome resistance in vitro and in vivo. Our study reveals a novel PP1-centered phospho-splicing circuit governing pro-survival autophagy in GBM and provides a mechanistically grounded, immediately translatable combination therapy to combat TMZ resistance. - Source: PubMed
Publication date: 2026/06/11
Fu HaijuanGao WeiGao AnboDeng KunLi DanyangHuang JianliangWang XiangyuWang BingWu Minghua - The metabotropic glutamate receptor 6 (mGluR6), encoded by , is a core component of the ON-bipolar signaling cascade in the retina, but its role in human retinal development remains unclear. Here, we used temporally controlled CRISPR-based genetic ablation in human induced pluripotent stem cell-derived retinal organoids to define the developmental functions of mGluR6. Unexpectedly, we found that mGluR6 is expressed not only in depolarizing ON-bipolar cells but also transiently in cone photoreceptors during human retinal development, a pattern not observed in the mouse retina. Early loss of prior to synaptogenesis disrupted cone pedicle architecture, leading to mislocalization of synaptic proteins including Bassoon, ELFN2, and TRPM1, and ultimately resulting in widening or duplication of the outer plexiform layer (OPL). In contrast, deletion after synapse formation did not alter OPL synapses or morphology, revealing a temporally restricted requirement for mGluR6 during circuit assembly. These findings uncover a previously unrecognized role for mGluR6 in coordinating cone terminal targeting and synaptic layer assembly during human retinal development and highlight the power of temporally controlled genetic manipulation in organoid systems to reveal species-specific mechanisms of neural circuit formation. - Source: PubMed
Publication date: 2026/04/27
Bahmani LeilaGalvan PatriciaHosseini HiradBai JinlunBharathan Sumitha PChen MichaelStepanian KaylaThornton Matthew EGrubbs Brendan HNagiel Aaron - Lymph node metastasis (LNM) is the most frequent metastatic pathway in gastric cancer (GC) and a major determinant of poor prognosis, but the underlying molecular mechanisms remain poorly defined. In this study, we investigated the role of extracellular leucine-rich repeat and fibronectin type III domain-containing protein 2 (ELFN2) in LNM and its therapeutic potential in GC. ELFN2 expression was examined in clinical GC tissues and found to be significantly downregulated in cases with LNM, with low ELFN2 levels correlating with unfavorable patient survival. Mechanistic studies demonstrated that ELFN2 interacts directly with the catalytic subunit alpha of protein phosphatase-1 (PP1A), thereby inhibiting YAP dephosphorylation at Ser127. This regulation promotes YAP nuclear export and functional inactivation. Pharmacological inhibition of PP1A abrogated ELFN2-induced YAP inactivation, confirming the requirement of PP1A in this process. To further validate the biological significance of ELFN2, we established in vivo models of LNM and peritoneal carcinomatosis, which consistently showed that ELFN2 suppresses metastatic dissemination. Together, our results reveal a novel ELFN2/PP1A/YAP signaling axis that plays a critical role in controlling LNM in GC. Importantly, these findings not only provide new insights into the molecular mechanisms governing GC metastasis but also highlight ELFN2 as a promising biomarker and potential therapeutic target for the management of GC patients at high risk of LNM. - Source: PubMed
Publication date: 2026/04/10
Ling RuoyuYang HuaZhang GuofanChen JingYe ZhaoGou LongfeiLei XuetaoYang QingbinPeng YanmeiYe GengtaiLi GuoxinChen Hao