HOMER2 antibody
- Known as:
- HOMER2 (anti-)
- Catalog number:
- orb100530
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- HOMER2 antibody
Related genes to: HOMER2 antibody
- Gene:
- HOMER2 NIH gene
- Name:
- homer scaffold protein 2
- Previous symbol:
- -
- Synonyms:
- CPD, Cupidin, Vesl-2, HOMER-2B, HOMER-2, HOMER-2A, DFNA68
- Chromosome:
- 15q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-28
- Date modifiied:
- 2018-03-01
Related products to: HOMER2 antibody
Related articles to: HOMER2 antibody
- HOMER proteins are scaffolding proteins critically involved in intracellular signaling, calcium homeostasis, receptor trafficking and synaptic plasticity. Three human HOMER genes (HOMER1, HOMER2, HOMER3) are expressed in both neurons and skeletal muscle fibers. HOMER1 long isoforms multimerize via their carboxy-terminal coiled-coil domain, forming signaling clusters with postsynaptic density proteins. Despite growing evidence of HOMER1 relevance in skeletal muscle physiology, molecular data on human muscle remain scarce. This study investigates the expression of alternatively spliced HOMER1 transcripts in human skeletal muscle, with focus on a previously uncharacterized intermediate isoform, HOMER1E. Human skeletal muscle biopsies (Soleus and Vastus Lateralis) and cerebellum were analyzed by RT-PCR and droplet digital PCR (ddPCR) to quantify HOMER1 transcript variants. HOMER1E cDNA was cloned and expressed in HEK293 cells alongside full-length HOMER1. Protein stability was assessed using cycloheximide chase assays. Degradation pathways were investigated with MG-132 (proteasome inhibitor) and Bafilomycin A1 (autophagy inhibitor). Protein-protein interactions were evaluated by co-affinity purification and confocal immunofluorescence. Structural modeling employed AlphaFold-Multimer and DeepCoil predictions. Three HOMER1 transcripts (HOMER1, HOMER1H, HOMER1E) were detected in human skeletal muscle, with HOMER1E representing ~ 0.2% of total HOMER1 transcripts, as determined by ddPCR. HOMER1E encodes a 224 aa, 25.8 kDa protein which lacks exons 4-6 (including the autoinhibitory P-motif) but retains both N- and C-termini. In HEK293 cells, HOMER1E protein was highly unstable, primarily degraded via autophagy, while co-expression with HOMER1 significantly stabilized it. Co-affinity purification and immunofluorescence confirmed direct HOMER1-HOMER1E interaction. Structural modeling predicted a coiled-coil-mediated antiparallel heterodimer interface. HOMER1E is a minor, unstable HOMER1 isoform in human skeletal muscle with no murine counterpart. Its interaction with full-length HOMER1 via the conserved coiled-coil domain, combined with its rapid autophagic turnover, suggests a regulatory role in modulating multimeric HOMER1 scaffolding under specific physiological or developmental conditions. - Source: PubMed
Publication date: 2026/08/27
Furlan SandraCarotti MarcelloSamaha AhmedMinervini GiovanniAkyurek Eylem EmekDazzo EmanuelaLorenzon PaolaBlottner DieterSalanova MicheleSandonà DoriannaVolpe Pompeo - HOMER family proteins are extensively expressed across human tissues, exhibiting aberrant expression patterns that are specific to tissues and diseases. HOMER1 has been linked to neurodevelopmental disorders, HOMER2 to hearing loss, and HOMER3 has been implicated in oncogenic processes across various malignancies [1, 2]. Homer Scaffold Protein 3 (HOMER3), a scaffold protein comprising 361 amino acids, is encoded on human chromosome 19p13.11. However, its role across different cancers remains inadequately characterized. This study aims to comprehensively evaluate the expression landscape, prognostic significance, drug sensitivity associations, and immune-related features of HOMER3 across diverse cancer types, with a particular focus on colorectal cancer (CRC), to support its potential as a prognostic biomarker and therapeutic target in CRC. - Source: PubMed
Publication date: 2026/07/07
Zhu Hong-ChaoXia KunWang WeiTian Hai-YangWang Nan - The central nervous system responds to acute injury with plastic remodeling of its network. However, the temporal and structural dynamics of this response in the denervated dentate gyrus remain poorly understood. Therefore, we examined the transcriptional programs activated after perforant path transection, focusing on the outer molecular layer (OML) and the granule cell layer (GCL). - Source: PubMed
Publication date: 2026/05/19
Schlaudraff JessicaDel Turco DomenicoKey JanaDeller ThomasAuburger Georg - INTRODUCTION: Sarcoidosis is an inflammatory disease driven by immune-mediated mechanisms, characterized by the formation of epithelioid cell granulomas and a wide range of clinical manifestations. Its phenotype is the result of a complex interplay of genetic and environmental factors, the precise roles and interactions of which remain poorly defined. AIM: To identify candidate genes and risk loci associated with sarcoidosis from large population datasets. To estimate the genetic heritability of the phenotype in selected ancestries. POPULATION AND METHODS: Public summary statistics from the FinnGen release 12 (European ancestry), pan UK BioBank Project (UKBB - European and African ancestry), Million Veteran Program (MVP - European and African ancestry), and Japan BioBank (East Asian ancestry) were included for European, African and multi-ancestry meta-analysis through sample size-based analysis. Novel risk loci and single nucleotide polymorphisms (SNPs) significantly associated with the disease were critically reviewed on the basis of the available literature. For each risk locus, SNPs highly correlated with the lead SNP were selected based on Combined Annotation Dependent Depletion (CADD) scores. Genetic heritability (h2) scores were obtained through ancestry-specific linkage-disequilibrium score calculation. RESULT: Overall 9659 cases (7559 European, 1880 African, 220 East Asian) and 1,665,804 controls (1,361,726 European, 126,411 African, 177,667 East Asian) were analysed. Nineteen and two risk loci were identified in European and African ancestry, respectively; h2 scores were 0.25 (European) and 0.19 (African). Candidate non-MHC genes for further explorations through functional studies included IL23R, PUS10, ACOXL, PLCL1, FAM117B, BMPR2, PPARG, ESYT2, ANXA11, CCDC88B, ATXN2, CCL24, RP11−540O11.1, HOMER2, CD19, UBASH3A, RNF215, and others. Interferon gamma signaling, meiotic recombination/condensation of prophase chromosomes, and DNA methylation were the most enriched gene sets in European and multi-ancestry meta-analysis. Multi-ancestry meta-analysis was confronted with FinnGen+UKBB+MVP meta-analysis (released by FinnGen freeze 12) yielding consistent results (18 risk loci identified) CONCLUSION: Nineteen and two risk loci were significantly associated with sarcoidosis for European and African ancestries, respectively. Moderate genetic heritability was observed for both ancestries. A set of significantly associated non-MHC genes and SNPs was obtained to investigate functional validation. Although further studies are warranted, epigenetic alterations may contribute to the risk of developing sarcoidosis - Source: PubMed
Publication date: 2025/12/29
Ricci AndreaAndolfi FedericaSabbatini DanieleGozzi FilippoBetto Giada DiVentura PaoloBuzzetti ElenaPietrangelo AntonelloClini EnricoTonelli RobertoAndrisani Dariode Guzman Marinduque Brent JuliusBergamini ElisaVecchi ChiaraPegoraro ElenaGregori DarioCorradini ElenaCerri Stefania - There is a lack of objective evaluation tools for assessing upper limb motor dysfunction in ischemic stroke patients (ULMD-IS). This study aimed to develop and validate a diagnostic nomogram for diagnosing the severity of ULMD-IS using functional near-infrared spectroscopy (fNIRS) data. - Source: PubMed
Publication date: 2025/12/04
Liu MenghuiWan ChunxiaoWang ChunyanLi XinyiShang Mengmeng