Ask about this productRelated genes to: ELMO1 antibody
- Gene:
- ELMO1 NIH gene
- Name:
- engulfment and cell motility 1
- Previous symbol:
- -
- Synonyms:
- KIAA0281, CED12, ELMO-1, CED-12
- Chromosome:
- 7p14.2-p14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-13
- Date modifiied:
- 2018-02-13
Related products to: ELMO1 antibody
Related articles to: ELMO1 antibody
- Oligodendroglial cells are the myelinating glial cells of the central nervous system (CNS), and their morphological differentiation is a prerequisite for efficient myelin formation, which is essential for proper neuronal function. While oligodendroglial morphological changes normally proceed through tightly regulated developmental transitions, disruption of the underlying molecular mechanisms can lead to aberrant cellular phenotypes characterized by either premature, insufficient, or excessive differentiation. Although the phosphatidylinositol 3-kinase (PI3K) and its downstream Akt kinase signaling are well established as major drivers of oligodendrocyte morphological differentiation, myelination, and CNS white matter formation, how its negative regulator, phosphatase and tensin homolog (PTEN), is involved in the regulation of oligodendroglial morphogenesis remains incompletely understood. Recent genetic studies have highlighted a spectrum of disorders caused by PTEN dysfunction, conceptually established but currently evolving as PTENopathy, which has been partially associated with white matter abnormalities. Here, we report that, in an experimental model using the FBD-102b cell line, a well-established model of oligodendroglial cell differentiation, chemical inhibition of PTEN enhances pronounced morphological changes characterized by widespread membranes, accompanied by increased expression of differentiation and/or myelin marker proteins. We then focused on Rho family small GTPases, central regulators of cell morphogenesis, and examined their potential involvement downstream of this signaling. Expression of the RhoG-binding domain (RBD) of engulfment and cell motility 1 (ELMO1) attenuated the increased morphological changes. Similarly, inhibition of downstream Akt signaling also reversed these changes. Taken together, these results provide insight into how balanced regulation between PTEN and downstream signaling molecules governs oligodendroglial cell differentiation and suggest that dysregulation of this signaling equilibrium may contribute to cellular phenotypes relevant to disease-associated cellular alterations. - Source: PubMed
Publication date: 2026/04/12
Takahashi MikitoTanaka MeiYako HidejiMiyamoto YukiYamauchi Junji - Gastric cancer (GC) is the fifth most prevalent cancer and the fifth leading cause of cancer-related mortality worldwide. The current gold standard for clinical diagnosis is gastroscopy, which, despite its high sensitivity and specificity, is limited by its invasive nature and high cost, making it unsuitable for large-scale screening. Furthermore, the diagnostic process lacks biomarkers that offer both high sensitivity and specificity. A screening model incorporating five methylation-based biomarkers (ELMO1, FGF12, NPY, SEPTIN9, ZNF671) was developed. Using these methylation profiles, GC risk prediction models were constructed employing Random Forest. - Source: PubMed
Publication date: 2026/04/25
Long FengyingXu YiWu KangFu XiaoyuGao TangjieLuo ShiyaDai LizhongChen Xiao-Ping - Acute kidney injury (AKI) is a sudden episode of kidney failure linked to a wide range of health conditions. High mortality in AKI highlights the need to identify new therapeutic approaches. Homeostasis in multicellular organisms is exquisitely regulated by phagocytosis of apoptotic cells, also known as 'efferocytosis'. Apoptotic cells are frequently observed at sites of inflammation, including in AKI. Engulfment and cell motility protein-1 (ELMO1) is a regulator of the actin cytoskeleton that promotes apoptotic cell removal by phagocytes during efferocytosis. Mutations in the human gene are linked with diabetic nephropathy and, in animal models of this disease, high ELMO1 levels promote renal dysfunction. However, the role of ELMO1 in AKI was not known. Here, we describe the links between and kidney pathology and test global and tissue-specific ELMO1-deficient mice in models of AKI. While global loss of expression did not impact the immediate loss of renal function after ischemia-reperfusion elicited AKI, ELMO1 deficiency resulted in increased tissue injury in AKI caused by cisplatin injection. Cisplatin induced robust renal cell apoptosis that was significantly elevated in mice with the global loss of ELMO1, but not in mice with the macrophage-specific deletion. Using primary cell culture and immunofluorescence approaches, we highlight the role of ELMO1 in efferocytosis by several renal cell types, suggesting possible additive effects during nephrotoxic injury. - Source: PubMed
Publication date: 2026/03/27
Baffert BlandineCholko MichalSabapathy VikramModhukuru PritikaHeath IsaacZheng ShuqiuGautam JitendraSchneider KevinSilverman LilyOkusa MarkSharma RahulArandjelovic Sanja - Renal ischemia/reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI), a potentially fatal syndrome characterized by a rapid decline in kidney function. The major cause of AKI is IRI. Our prior studies have demonstrated that genetically increased Elmo1 expression in mice aggravated several kidney pathologies including diabetic nephropathy and transition of AKI to chronic kidney disease induced by IRI. However, the effects of decreased expression of Elmo1 on IRI is unclear. We compared the kidney structures and functions between wild type (WT) mice and mice with genetically decreased Elmo1 expression ( ) 5 days after unilateral renal IR surgery. The WT-IRI mice had typical tubular injuries including necrosis and shedding of proximal tubular cells, but these morphological changes were less severe in -IRI mice. In contrast, the urinary albumin excretion was elevated in -IRI mice compared with WT counterparts. While the expression of inflammatory markers (e.g., and ) was comparable between WT and mice with IRI which significantly higher than control mice, the expression of antioxidant markers (e.g., and ) was preserved in -IRI mice which was significantly decreased in WT-IRI mice. We conclude that mice had preserved tubular structures but increased urinary albumin excretion after IRI, suggesting that the role of Elmo1 in IRI is complex and it merits future evaluation. - Source: PubMed
Publication date: 2026/02/27
Chen MeitongMa QingWariyapperuma Appuhamillage Niroshani M WWang YuyeKayashima YukakoMaeda-Smithies NobuyoLi Feng - The genetic architecture of Parkinson's disease (PD) and progression to PD dementia (PDD) remains incompletely characterized in Asians. Here, we investigated genetic risk factors for PD and PDD in Taiwanese individuals from the Taiwan Precision Medicine Initiative (TPMI), the largest non-European cohort integrating genetic and electronic medical record data. - Source: PubMed
Publication date: 2026/03/04
Lin Chin-HsienChang Chien-ChingChen Hung-HsinLin Wan-JiaHsu Chia-LangLin Rung-JuenGuo Yi-JenFang Ting-ChunLin Shinn-ZongHuang Chih-YangWang Shuu-JiunHang Jen-FanHsieh Sun-WungChou Mei-ChuanYeh Tu-HsuehHu Chaur-JongYang Fu-ChiChang Hsin-AnLee Tsong-HaiTsai Meng-HanKuo Ming-CheLiou Jyh-MingWu Ming-ShiangPark Kye WonChung Sun JuTan Eng-KingShen-Jang Fann Cathy