Ask about this productRelated genes to: Homer1 antibody
- Gene:
- HOMER1 NIH gene
- Name:
- homer scaffold protein 1
- Previous symbol:
- -
- Synonyms:
- Ves-1, SYN47, HOMER-1B
- Chromosome:
- 5q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-28
- Date modifiied:
- 2018-03-01
Related products to: Homer1 antibody
Related articles to: Homer1 antibody
- Homer proteins (Homer1-3) are scaffold proteins that mediate protein-protein interactions in signal transduction; however, the role of Homer3 in breast cancer (BC), particularly triple-negative breast cancer (TNBC), remains poorly defined. Here, we investigated the clinical relevance and functional significance of Homer3 in BC and TNBC. Publicly available datasets from TCGA and GEO were analyzed to evaluate associations between Homer3 expression and patient outcomes using Kaplan-Meier survival analysis. Pathway enrichment analysis and gene set variation analysis (GSVA) were performed to identify signaling programs associated with Homer3 co-expressed genes. Functional roles were examined using stable TNBC cell lines with Homer3 knockdown or overexpression, followed by assays for cell proliferation, clonogenic growth, migration, invasion, and wound healing. We found that Homer3 expression was elevated in breast tumors compared with normal tissues and was associated with poor prognosis in both BC and TNBC. Homer3 expression was higher in TNBC than in non-TNBC subtypes and negatively correlated with estrogen receptor (ER) and progesterone receptor (PR) expression. Functionally, Homer3 depletion suppressed TNBC cell proliferation, clonogenic capacity, migration, invasion, and wound healing, whereas Homer3 overexpression produced reciprocal effects. Pathway analyses revealed that Homer3 co-expressed genes were enriched in cell cycle-related pathways and Hallmark MYC signaling, which were associated with adverse clinical outcomes. Consistently, Homer3 knockdown selectively reduced key proliferative cell-cycle regulators. Collectively, these findings demonstrate that Homer3 is associated with aggressive phenotypes and MYC- and cell cycle-linked proliferative programs in breast cancer, particularly in TNBC. Survival analyses are presented as exploratory findings, supporting the biological relevance of Homer3 in TNBC. These findings suggest that Homer3 may represent a potential therapeutic vulnerability. - Source: PubMed
Publication date: 2026/08/04
Tsai Kuei-YenChang Yu-JiaLin Jang-ChunPrince G M Shazzad HossainBatzorig UyangaLee Ai-WeiHung Chin-Sheng - Melatonin (Mel) exerts antioxidant and anti-ferroptosis effects not only via the canonical receptors Mt1/Mt2 but also via metabotropic glutamate receptor 1 (mGluR1)/glutamate-mediated signaling. Nevertheless, the regulatory mechanism by which Mel modulates mGluR1/glutamate signaling in retinal ischemia-reperfusion (I/R) injury and its downstream effects on ferroptosis and oxidative stress remain poorly understood. Here, bulk RNA sequencing identified that the Mel receptors Mt1/Mt2 and ferroptosis/iron-redox regulators (Gpx4, Fth1, and xCT) were significantly downregulated after retinal I/R. Mel improved retinal structural and visual function, visual-guidance behavior, and electrophysiological responses following I/R while concurrently reducing ferroptotic and inflammatory injury markers. These benefits were largely abolished by Mel membrane receptor antagonists. Mechanistically, Mel upregulated Homer1a in vivo and in vitro in a receptor-dependent manner. Conditional deletion of Homer1a in transgenic mice, as well as Homer1a knockdown in retinal ganglion cells (RGCs), abolished the protective effects of Mel on visual function, along with its anti-ferroptotic and anti-inflammatory activities. Molecular docking and immunoprecipitation assays demonstrated that Mel restored the interaction between Homer1a and mGluR1 and activated the xCT/GSH/Gpx4 antioxidant axis. Pharmacologic inhibition of xCT with the buthionine sulfoximine (BSO) simulation pr genetic interference with xCT expression counteracted the protective effects of Mel. Mel also enhanced Nrf2-mediated transcriptional expression of cCT in a Homer1a/mGluR1-dependent manner. Collectively, our results define a Mel-Homer1a/mGluR1-Nrf2/xCT signaling cascade that promotes RGCs survival after I/R by suppressing ferroptosis/iron-redox reactions, thereby providing a potential translatable strategy for receptor-targeted intervention in I/R-related retinal damage. - Source: PubMed
Publication date: 2026/07/10
Dou Ya-NanWen YuwenHuang YuanWu XiuquanZhang ZehanWang GuanyiChao WangshuWei DongyuLv WeihaoFei XiaoweiFei ZhouFei Fei - 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 - This study investigated whether electroacupuncture at "Zhisanzhen" (EA-ZSZ) alleviates cognitive impairment in vascular dementia (VD) rats by regulating the astrocyte-synapse axis, reshaping the hippocampal secretory microenvironment, and preserving synaptic structural integrity. - Source: PubMed
Guo SijingLiu QianLin ShihaoZhou TaotaoHu QinTang Zhongsheng - Cerebral edema (CE) is a major determinant of poor outcomes after traumatic brain injury (TBI). CE affects approximately 60% of patients with mass lesions on head computed tomography (hCT) and confers a tenfold increase in mortality. Despite this burden, no validated biomarkers exist to identify patients at risk for early CE worsening or to elucidate the biological processes underlying divergent edema trajectories. We conducted high-throughput plasma proteomic profiling in a prospective moderate-severe TBI cohort with evidence of intracranial blood on the initial post-injury hCT scan (n=123 patients) to (1) identify a clinically feasible set of biomarkers plus a predictive model that could be used to assess CE risk at admission, and (2) conduct a mechanistic, hypothesis-generating analysis to identify the molecular networks involved in CE progression in the first hours post-injury. Plasma collected within 3 hours of injury was analyzed using the Olink Explore platform (5394 proteins), and patients underwent head CT imaging upon presentation and at 6 hours. Two complementary analytic pathways, reflecting the study's two goals, were pursued in parallel. First, logistic regression with false discovery rate (FDR) correction identified a conservative 12-protein set associated with baseline CE. When combined with targeted clinical variables (i.e., age, sex, admission GCS, pupil reactivity, admission glucose, admission alcohol), this panel supported high-performing supervised classifiers for predicting CE worsening by 6 hours post-baseline scan (best model: XGBoost, AUC = 0.78; recall = 0.83). Second, a broader 60-protein panel, selected via bootstrapped elastic-net regression, was used to interrogate the mechanistic architecture of CE worsening using random forest SHAP attribution and protein-protein interaction modeling. Proteomic signatures diverged sharply between patients whose CE did and did not worsen. The CE worsening group was characterized by a coherent neuronal-synaptic injury axis dominated by ELAVL4, CEND1, NEFL, NECAB2, GFAP, CHGB, RPH3A, HPCAL4, and HOMER1, proteins involved in neuronal structural integrity, vesicular trafficking, synaptic vesicle cycling, calcium signaling, and axonal degeneration. These reciprocal proteomic states suggest that early edema progression may be driven by coordinated disruption of neuronal and synaptic resilience programs. Together, these findings suggest (1) a hyperacute biomarker panel plus predictive model with potential for prospective validation and (2) mechanistic evidence for a distinct neuronal-synaptic injury network that associates with early edema worsening after TBI. - Source: PubMed
Publication date: 2026/05/26
Radabaugh Hannah LAbdelhak AhmedNing KiarraJha Ruchira MRowell Susan EPollock Jeffrey MMendoza EsmeraldaRojas Valencia Luisa MFerguson Adam RHinson H E