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
- 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 - The EVH1 domain of the Homer1 scaffold protein interacts with the proline-rich region of Shank3, forming a key network within the postsynaptic density. While two mutations (M65I and S97L) in the EVH1 domain have been suggested to be associated with autism spectrum disorder, our results show that neither mutation has a substantial effect on the overall structure or the partner binding properties of Homer1. Compared to the S97L variant, the M65I mutant exhibits larger chemical shift perturbations both upon the mutation itself and during partner binding, while also showing signs of thermal destabilization. Finally, integration of computational and NMR data suggests that both mutations perturb the μs-ms timescale internal motions of the EVH1 domain. - Source: PubMed
Publication date: 2026/05/28
Farkas FanniMaruzs BrigittaKálmán Zsófia EKlumpler TomasBatta GyulaPéterfia BálintGáspári Zoltán - Women experience nearly twice the prevalence of depression compared to men and frequently present with comorbid anxiety, with this divergence emerging during adolescence. However, the molecular mechanisms underlying female-specific depression vulnerability remain poorly understood. Here, we found that prenatal stress (PS) induced depressive-like behaviors and selectively downregulated Slit Guidance Ligand 1 (Slit1) expression in the hippocampal dentate gyrus (DG) of female adolescent offspring rats. Furthermore, viral knockdown of Slit1 in the DG induced anxiety- and depressive-like behavioral phenotypes specifically in female rats. In females, Slit1 deficiency reduced the mean fluorescence intensity of the neural stem cell and immature neuron markers Sox2 and DCX in the DG, decreased postsynaptic Homer1, PSD95, and GluA1 expression without affecting Synaptophysin, and diminished the amplitude of sEPSCs. Significantly, the downstream Slit1 effector SLIT-ROBO Rho GTPase-activating protein 2 (Srgap2) was downregulated specifically in Slit1-deficient females. Together, these results suggest that Slit1 disruption selectively affects DG neuroplasticity in females and may contribute to their heightened vulnerability to PS-related depressive-like behaviors, although further mechanistic studies are required to confirm the causal role of Slit1 in these effects. - Source: PubMed
Publication date: 2026/05/08
Xu KaixuanChen TuYang YangLiu WeiminGuo HuanGong ZhengMa XinyiLiu JiajiaLu YushanZhang HuipingFan XiaotangLi HuiZhu Zhongliang - Perioperative neurocognitive disorders (PNDs) are common complications in elderly surgical patients. Possible pathogenic mechanisms for the development of PNDs include loss of synaptic connections mediated by microglial activation, although the precise mechanisms are not fully understood. - Source: PubMed
Publication date: 2026/05/06
Lv JingjingYao LiangTang LiliLi QibingWang LixiaYan XunchuanLi MengmengPeng WenjingZhang HuiwenGuo JiaxinWeng JuntaoMei BinZhang JiqianYang ZhilaiShen QiyingLu YaoChen YongquanHu JunMaze MervynLiu Xuesheng