Ask about this productRelated genes to: LIMK1 antibody
- Gene:
- LIMK1 NIH gene
- Name:
- LIM domain kinase 1
- Previous symbol:
- -
- Synonyms:
- LIMK
- Chromosome:
- 7q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1996-03-14
- Date modifiied:
- 2015-09-03
Related products to: LIMK1 antibody
Related articles to: LIMK1 antibody
- Sensorineural hearing loss (SNHL) is a prevalent clinical disorder in otorhinolaryngology, with cochlear ischemia/reperfusion (I/R) injury-induced hair cell apoptosis being a core pathogenic mechanism. Ginsenoside Rb1 (Rb1), a major active component of Panax ginseng, exhibits potent anti-apoptotic and neuroprotective effects, but its role and underlying mechanism in cochlear I/R injury remain elusive. - Source: PubMed
Publication date: 2026/09/05
Chang WeiHuang JiangLiao QiongYang XinzhuBin JiWu Wenke - Breast cancer (BC) is the most commonly diagnosed malignancy in women, with triple-negative breast cancer (TNBC) representing the most aggressive subtype that is associated with poor clinical outcomes. Identifying novel biomarkers or therapeutic targets is therefore of great importance. Nectin cell adhesion molecule-2 (NECTIN2) is an immunoglobulin-like glycoprotein involved in cell adhesion and immune regulation that is highly expressed in several cancers but its role in the progression of BC is unclear. Using publicly available data sets, we found that NECTIN2 expression is elevated in BC compared to normal tissues and is associated with poorer recurrence-free survival in TNBC patients. Among TNBC cell lines, MDA-MB-231 cells exhibited the highest expression of NECTIN2 at gene and protein levels, consistent with a more aggressive phenotype. To investigate its functional role, we silenced NECTIN2 in MDA-MB-231 and MDA-MB-468 cells. Relative cell viability was modestly reduced in NECTIN2-depleted MDA-MB-231 cells at later time points, but no significant changes were observed in MDA-MB-468 cells. Interestingly, NECTIN2 depletion significantly reduced migration and invasion in MDA-MB-231 cells, but not in MDA-MB-468 cells. Given this cell line-specific effect, subsequent mechanistic investigations focused on the MDA-MB-231 model. Gene expression profiling suggested a reduction in LIMK1, a regulator of cytoskeletal dynamics and cell motility, following NECTIN2 depletion. Furthermore, ectopic expression of LIMK1 in NECTIN2-deficient MDA-MB-231 cells partially restored migratory capacity and was associated with partial epithelial-mesenchymal transition (EMT)-like changes, including a decrease in E-cadherin and ZO-1, and a higher level of fibronectin and Slug. Collectively, these findings suggest that NECTIN2 contributes to migratory and invasive phenotypes in MDA-MB-231 cells, potentially through LIMK1-associated cytoskeletal remodeling and EMT-related marker changes. However, this mechanism requires further investigation because it appears to be context-dependent and may not be universally applicable across TNBC subtypes. - Source: PubMed
Publication date: 2026/08/28
Klaihmon PhatchanatMuangtate PattaratornThongphayong SudaratSaetan PuretatChanthateyanonth SupasornThuwajit ChanitraIssargrisil SurapolPhannasil Phatchariya - Type 1 diabetes (T1D) is a systemic metabolic disorder associated with male reproductive dysfunction. Given the pivotal role of actin cytoskeleton remodeling in spermatogenesis and sperm function, this study investigated the effects of T1D on actin-regulating pathways in rat testis and spermatozoa (SPZ). Adult Wistar rats were rendered diabetic by streptozotocin administration (65 mg/kg, i.p.). Testicular analysis revealed a reduced F-/G-actin ratio together with marked F-actin disorganization, consistent with altered actin cytoskeleton remodeling. To investigate the molecular mechanisms underlying these alterations, key regulators of actin dynamics were examined. Diabetic animals displayed impaired expression of EPS8, Fascin, N-WASP, and the ARP2/3 complex, suggesting altered regulation of actin assembly, bundling, and branching. Further analyses demonstrated dysregulation of signaling pathways governing cytoskeletal organization. Reduced levels of phosphorylated Disheveled-2, DAAM1, RhoA-GTP, and ROCK1 indicated impairment of the planar cell polarity pathway. In parallel, changes in LIMK1/cofilin phosphorylation supported abnormal regulation of actin filament turnover. Alterations in the RICTOR/PKC/MARCKS signaling pathway further highlighted defects in cytoskeletal control. Similar abnormalities were observed in mature SPZ, where altered F-actin distribution and DAAM1 localization suggested persistent cytoskeletal defects. Moreover, diabetic SPZ exhibited a reduced ability to undergo acrosome reaction, accompanied by altered MARCKS phosphorylation, highlighting defects in actin-dependent processes essential for sperm function and fertilizing capacity. These findings indicate that disruption of actin cytoskeleton dynamics may represent a major mechanism contributing to testicular and sperm abnormalities in T1D, providing new insights into the mechanisms underlying diabetes-associated male reproductive dysfunction. - Source: PubMed
Publication date: 2026/08/19
Ambruosi Maria RosariaBiasi AlessandraBoccella SerenaRomdhani IlefFalvo SaraGuida FrancescaMaione SabatinoMinucci SergioVenditti Massimo - Inflammatory bowel disease (IBD) involves complex immunometabolic dysregulation. Mitochondria-associated endoplasmic reticulum membranes (MAMs) link metabolic adaptation and inflammatory signaling, but gene expression features associated with MAM-related transcriptomic states in IBD remain unclear. Public transcriptomic datasets were integrated with a curated MAM-related gene set and herbal target information. Differential expression analysis, weighted gene coexpression network analysis, and machine learning-assisted feature selection were used to identify candidate genes. A two-gene nomogram was constructed and evaluated in discovery and independent validation datasets. Functional enrichment, immune deconvolution, regulatory network prediction, molecular docking, 200-ns molecular dynamics simulations, and preliminary quantitative polymerase chain reaction validation were performed. and were identified as candidate transcriptomic signature genes associated with IBD status and MAM-related transcriptional states, showing discriminatory performance in independent datasets. Both genes were associated with cytokine-cytokine receptor interaction and drug metabolism-cytochrome P450 pathways and were linked to macrophage-related immune states. Structural analyses suggested stable predicted binding between and 1-(4-hydroxybenzyl)-4-methoxy-9,10-dihydrophenanthrene-2,7-diol and structurally plausible interactions between and palmatine. Preliminary tissue-level validation supported the disease-associated expression pattern of , whereas showed a consistent but nonsignificant upward trend. and may represent candidate transcriptomic signatures associated with MAM-related regulatory states in IBD. These findings should be interpreted as hypothesis-generating associations rather than evidence of MAM localization, functional causality, or therapeutic efficacy. Further protein-level and functional validation is required. - Source: PubMed
Publication date: 2026/08/12
Tu HoushuChen MenglinZhu PanpanHe LingHong Jing - Based on a strategy integrating topological feature identification and path priority assessment, this study systematically explored the efficacy targets and differentiated mechanisms of Colquhounia Root Tablets(CRT) in the "homotherapy for heteropathy" of rheumatoid arthritis(RA) and diabetic kidney disease(DKD). Firstly, candidate targets of CRT and disease-specific genes were retrieved by integrating multi-source databases and transcriptomic data. Protein-protein interaction(PPI) networks were constructed to identify key targets shared by or specific to RA and DKD via topological feature identification. Subsequently, a path priority assessment was introduced to calculate the average shortest path(ASP) values from drug targets to various pathological segments, thereby quantifying intervention efficacy to lock onto "dominant pharmacodynamic links". The predicted key functional axes were validated through animal experiments. The results indicated that the core targets of CRT for both diseases involved shared pathways such as phosphatidylinositol 3-kinase(PI3K)-protein kinase B(Akt), tumor necrosis factor(TNF), and glycolysis/gluconeogenesis. Notably, path priority assessment revealed distinct dominant intervention links: for RA, CRT preferentially targeted "fibroblast-like synoviocyte(FLS) activation and invasion"(ASP=2.361), which mapped to the TNF-p38 mitogen-activated protein kinase(p38)-LIM domain kinase 1(LIMK1)-Cofilin1 axis to regulate cytoskeleton remodeling; for DKD, the dominant link was "filtration barrier injury and interstitial fibrosis"(ASP=2.295), converging on the TNF-poly(ADP-ribose) polymerase 1(PARP1)-signal transducer and activator of transcription 1(STAT1)-matrix metallopeptidase 9(MMP9) axis to mediate cellular senescence and senescence-associated secretory phenotype(SASP) secretion. Animal experiments confirmed that CRT significantly alleviated RA synovial invasion and DKD renal fibrosis by inhibiting these two differentiated signaling axes, respectively. By employing topological feature identification and path priority assessment, this study elucidates the scientific connotation of "homotherapy for heteropathy" of RA and DKD with CRT through both shared network regulation and intervention in disease-specific differential signaling axes associated with pharmacodynamic links. - Source: PubMed
Cai Bing-BingMao XiaMa Zhao-ChenXu Ming-ZhuLin YaLin NaZhang Yan-Qiong