Ask about this productRelated genes to: TMOD1 antibody
- Gene:
- TMOD1 NIH gene
- Name:
- tropomodulin 1
- Previous symbol:
- D9S57E, TMOD
- Synonyms:
- ETMOD
- Chromosome:
- 9q22.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-21
- Date modifiied:
- 2016-10-05
Related products to: TMOD1 antibody
Related articles to: TMOD1 antibody
- Cyclase-associated actin cytoskeleton regulatory protein 2 (CAP2) is a conserved actin-binding protein that promotes actin filament (F-actin) turnover by disassembling ADF/cofilin-decorated filaments, supporting F-actin remodeling in differentiating cells and tissues. In the ocular lens, the actin cytoskeleton is critical for maintaining tissue biomechanical properties during fiber cell maturation. To assess CAP2's role in the lens, we examined lens-specific CAP2 knockout ( ) mice at cellular and tissue levels. lenses were normal in size, shape, and transparency but exhibited increased stiffness under compression and enhanced recovery after load removal. While total actin levels and F-actin were unchanged, immunofluorescence revealed higher levels of Tropomodulin 1 (Tmod1, F-actin pointed-end capping), Tropomyosin3.5 (Tpm3.5, F-actin stabilizing), and T-plastin (F-actin bundling) in F-actin-rich membrane protrusions of mature fibers, while α-actinin-1 (F-actin cross-linking) was reduced. These findings suggest that CAP2 loss disrupts F-actin remodeling, promoting filament stabilization through Tpm3.5 binding, Tmod1 capping and T-plastin bundling. Consequently, F-actin networks become stiffer and more resilient, altering lens biomechanics. This study provides the first evidence that CAP2 regulates cell biomechanical properties in a non-muscle tissue through modulation of F-actin-associated proteins. - Source: PubMed
Publication date: 2025/10/15
Cheheltani SepidehCoffin MeganFowler Velia M - Tropomodulins (TMODs) are a group of proteins that stabilize the actin filament network by capping the slow-growing end of F-actin. Although their roles in tissue morphogenesis have been extensively studied in triploblastic organisms, their function in diploblastic remained unexplored. This study identified that in , expression is strongly upregulated in ectodermal cells at the parent-offspring junction during basal constriction formation and bud detachment. Notably, siRNA-mediated knockdown inhibits basal constriction formation, a pre-requisite morphological event for bud detachment. knockdown polyps show fragmented stress fibers and altered cell morphology adjacent to the basal constriction site. Finally, pharmacological studies showed that FGFR signaling is necessary for expression. Collectively, our results establish that Hydra is an FGFR-ERK2 signaling-regulated gene that is exclusively expressed in the epitheliomuscular ectodermal cells at the parent-offspring junction and is essential for bud separation from the parent polyp by promoting F-actin polymerization/stabilization. - Source: PubMed
Publication date: 2025/10/15
Kulkarni ShravaniMaity ShreyaTadasare NirajJoshi BhagyashriWagh GaneshBhakta SwarnavPatra Chinmoy - Tropomodulin-1 (TMOD1) is a key regulator of actin filament dynamics that functions as an actin-binding protein. It specifically caps the slow-growing (pointed) ends of actin filaments, and the interaction is further stabilized by tropomyosin (TPM). By modulating actin monomer polymerization and depolymerization, TMOD1 critically controls filament length, thereby maintaining both the stability and plasticity of actin-based structures. Emerging evidence has highlighted the participation of TMOD1 in diverse cellular processes, such as cytoskeletal organization, neurite outgrowth, cell motility, and cancer progression. This review summarizes recent advances in TMOD1 research and offers a comprehensive overview of its multifaceted biological roles and implications for future studies. - Source: PubMed
Publication date: 2025/10/22
Li YalongPan XuyiGong ZixuanZhu LinMu PingLu Fangjin - Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer (BC), characterized by poor clinical behaviors and outcomes. TMOD1 was reported as a downstream target of NF-κB contributing to the growth of cancer cells. However, it's impacts on TNBC patients' prognosis and treatment response remain unclear. - Source: PubMed
Publication date: 2025/10/16
Li YijieLong XinyiXie YitingZhong XiaorongCao ShiyuChen FeiShen MengjiaXiao LinYin LijuanYe FengLuo Ting - Actin dynamics are crucial for the morphogenesis and function of neurons in the brain. Tropomodulins (Tmods) belong to a family of actin-binding proteins that cap the pointed-end of actin filaments. There are four Tmod isoforms, and three of which, Tmod1, Tmod2 and Tmod3, are expressed in the brain, with Tmod2 exhibiting neuronal specific expression. By regulating actin filament dynamics, Tmods participate in neurite outgrowth, dendritic spine formation, and synaptic morphology, thereby contributing to structural and functional neural plasticity. Dysregulation of Tmods has been demonstrated in several neurodegenerative and neuropsychiatric diseases, such as Alzheimer's disease, epilepsy, Down syndrome, and addictive behaviors. Currently, compared to cancer and cardiovascular diseases, the roles and mechanisms of altered Tmod expression in neurological diseases remain poorly understood. In this article, we provided an overview on the physiological roles and crucial functions of Tmods in the brain, summarized the recent advances in alterations of Tmods in neurodegenerative and neuropsychiatric diseases, and discussed their implications and potential contributions to disease pathology and treatment. This review may expedite future studies to delineate the roles and molecular mechanisms of Tmods in brain physiology and pathology, ultimately promoting the development of novel diagnostic and therapeutic strategies for related neurological diseases. - Source: PubMed
Publication date: 2025/06/13
Hong ChuanLiu XiaopengZhou ZhouXing YuanCao ZixuanChang Yan-ZhongGao Guofen