|CSC-DC004866||Panoply™ Human ELMO1 Knockdown Stable Cell Line||Inquriy|
|CSC-SC004866||Panoply™ Human ELMO1 Over-expressing Stable Cell Line||Inquriy|
|CDCB157580||Human ELMO1 ORF clone (BC114341)||Inquriy|
|CDCB163094||Chicken ELMO1 ORF Clone (NM_001030994)||Inquriy|
|CDCB179678||Danio rerio ELMO1 ORF Clone (NM_213091)||Inquriy|
|CDCB186626||Rabbit ELMO1 ORF clone (XM_008261650.1)||Inquriy|
|CDCR059910||Human ELMO1 ORF clone (NM_001039459.2)||Inquriy|
|CDCR264734||Mouse Elmo1 ORF Clone(NM_080288.2)||Inquriy|
|CDCR375074||Rat Elmo1 ORF Clone(NM_001108415.1)||Inquriy|
|CDCS406949||Human ELMO1 ORF Clone (BC003051)||Inquriy|
|CDCS406950||Human ELMO1 ORF Clone (BC114341)||Inquriy|
|CDFR008033||Rat Elmo1 cDNA Clone(NM_001108415.1)||Inquriy|
|MiUTR3H-08436||ELMO1 miRNA 3'UTR clone||Inquriy|
|MiUTR3H-08437||ELMO1 miRNA 3'UTR clone||Inquriy|
Engulfment and cell motility 1(ELMO1), is a very conserved protein that mediates phagocytosis, migration and morphological changes in cells. ELMO1 is important for maintaining the homeostasis of organisms, and its abnormal expression is closely related to the clinical stage and prognosis of diabetic nephropathy, microbial infection, and malignant tumor. ELMO1 has been confirmed to be one of the sensitive genes of diabetic nephropathy and is also involved in the invasion and metastasis of tumor cells.
The Biological Role of ELMO1
The role of ELMO1 can be mainly reflected in the following aspects: (1) acting as a downstream substance of phosphatidylserine receptor cerebrovascular angiogenesis inhibitor 1 (BAI1) and synergizes with DOCK1 to activate the Rac1 downstream signaling pathway via Rac-GEF pathway, triggering cytoskeletal rearrangement and promoting integrin-mediated phagocytosis.; (2) promoting internalization of dead cells; (3) promoting neuronal growth factor-induced neurite outgrowth and participating in the morphogenesis of neuronal cells; (4) recruiting microtubule microfilament cross-linking factors on the surface of cell membranes to promote tubulin capture and ubiquitin-mediated formation of cellular pseudopods; (5) acting as a target for distant-less homeobox 1, Dlx1, and is selectively expressed in Reelin-positive [Re(+)] and Calretinin-positive [Cr(+)] interneurons, which are indispensable for the migration of activity-dependent intermediate neurons; (6) acting as a unique regulator of the endogenous mediator complex 31 (Med31), which is mainly located in the nucleus, increasing the expression of Med31 in the cytoplasm, promoting its ubiquitination, and jointly affecting the expression of cytokines IL10 and IL33.
Figure 1. ELMO1 directly transduces GPCR signaling to Rac1 to regulate F-actin dynamics in chemotaxing cells. (Youhong, et al. 2016)
ELMO1 and Diabetic Nephropathy
ELMO1 plays an important role in the pathogenesis of diabetic nephropathy (DN). Genome-wide association analysis (GWAS) and GoKinD study of Japanese (yellow), African American (black) and Caucasians (white) showed that mutations at the ELMO1 gene locus were associated with diabetic nephropathy. Genetic mutations in ELMO1 will result in increased expression of ELMO1 in the glomeruli of diabetic patients. The polymorphism site associated with DN of ELMO1 is at its transcription start position. The genetic polymorphism of ELMO1 is closely related to the development of glomerulosclerosis and the fibrosis process of the kidney under high glucose conditions. In addition, ELMO1 not only predicts the onset of kidney damage in diabetic nephropathy, but may also lead to kidney failure.
ELMO1 and Tumor Invasive Growth
ELMO1 is abnormally expressed in various malignant tumors including lung cancer, breast cancer, esophageal adenocarcinoma, ovarian cancer, thyroid cancer, rhabdomyosarcoma and glioma, and is closely related to the clinical stage and prognosis of the tumor. It is one of the genes associated with tumor cell migration.
Overexpression of ELMO1 was significantly positively correlated with the invasiveness of rhabdomyosarcoma. In ovarian cancer cell line SKOV3, downregulation of ELMO1 interacting protein DOCK180 directly leads to down-regulation of ELMO1, and cell proliferation, migration ability, and invasiveness are significantly inhibited, accompanied by changes in cell morphology, such as flaky pseudopodia and decreased formation of filopodia, suggesting that ELMO1 and DOCK180 support each other and synergistically stimulate the downstream effector Rac1, which regulates the malignant behavior of cell motility and ovarian cancer cells. Breast cancer studies have shown that expression of ELMO1 is associated with lymph node and distant metastasis, and knockout of ELMO1 can lead to lung metastasis in breast cancer.
Our promise to you:
Guaranteed product quality, expert customer support.
Contact us today for a free consultation with the scientific team and discover how Creative Biogene can be a valuable resource and partner for your organization.