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SH3GL1 encodes a member of the endophilin family of Src homology 3 domain-containing proteins.
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Our study provides novel evidence of Endo II function in HER2 (show ERBB2 ELISA Kits)+ cancer cell motility and trafficking of HER2 (show ERBB2 ELISA Kits) that relates to effective treatments with trastuzumab or T-DM1 (show DMPK ELISA Kits). Thus, differential expression of Endo II may relate to sensitivity or resistance to trastuzumab-based therapies for HER2 (show ERBB2 ELISA Kits)+ cancers
Expression level of SH3GL1 was widely upregulated in human OS tissues, and their overexpression was significantly correlated with more aggressive clinicopathological features.
Endophilin-A2 was identified as a novel molecule regulating macrophage-derived foam cell formation by mechanisms attributable to clathrin-mediated endocytosis and beyond clathrin-mediated endocytosis
inhibition of SH3GL1 reverses multidrug resistance through declining P-glycoprotein expression via the EGFR (show EGFR ELISA Kits)/ERK (show EPHB2 ELISA Kits)/AP-1 (show FOSB ELISA Kits) pathway.
results establish a novel function of endoA2 in clathrin-independent endocytosis
these data suggest that EEN may play a pivotal role in excessive cell proliferation and insufficient cell apoptosis of bone marrow plasma cells in multiple myeloma.
MIR218 functions as a tumor suppressor by regulating SH3GL1 expression in medulloblastoma cancer cells.
SH3GL1 may be involved in the oncogenic process of gliomas and effectively elicit an autologous antibody response in low-grade gliomas.
Two endophilin A2 mutants, E264A and E264R, have different effects on how endophilin interacts with other proteins, such as dynamin (show DNM1 ELISA Kits) or beta1-adrenergic receptors.
Idiopathic scoliosis is a multifactorial genetic disease and SH3GL1 may be one of the pathogenic genes for this disease.
This study provides a new mechanism by which endophilin A2 regulates ClC-3 (show CLCN3 ELISA Kits) channel activity, and sheds light on how ClC-3 (show CLCN3 ELISA Kits) is transported to cell membranes to play its critical role as a chloride channel (show CLCA1 ELISA Kits) in VSMCs function
Mutation in the FAK (show PTK2 ELISA Kits) gene disrupted the function of FAK (show PTK2 ELISA Kits) scaffolding to mediate endophilin A2 phosphorylation at Tyr (show TYR ELISA Kits)-315 by Src (show SRC ELISA Kits), leading to the decreased surface expression of MT1-MMP (show MMP14 ELISA Kits).
these results demonstrate that MNSFbeta/endophilin II inhibits the signal pathway upstream of IKK activation, but not downstream of TLR2 signaling.
Further analysis based on antibody staining of central and peripheral nerves revealed beta-adducin (show ADD2 ELISA Kits), septin 2, and sh3p8 as putative paranodal proteins.
Mll(Een/+) chimeric mice developed leukaemia displaying enlarged livers, spleens, thymuses and lymph nodes owing to infiltration of Mll(Een/+)-expressing leukemic cells
post-translational modification of endophilin II by MNSFbeta (show FAU ELISA Kits) might be implicated in phagocytosis by macrophages.
This gene encodes a member of the endophilin family of Src homology 3 domain-containing proteins. The encoded protein is involved in endocytosis and may also play a role in the cell cycle. Overexpression of this gene may play a role in leukemogenesis, and the encoded protein has been implicated in acute myeloid leukemia as a fusion partner of the myeloid-lymphoid leukemia protein. Pseudogenes of this gene are located on the long arm of chromosomes 11 and 17. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
SH3-domain GRB2-like 1
, EEN fusion partner of MLL
, SH3 domain protein 2B
, SH3 domain-containing GRB2-like protein 1
, SH3-containing Grb-2-like 1 protein
, extra 11-19 leukemia fusion
, extra eleven-nineteen leukemia fusion gene protein
, endophilin II
, SH3 domain-containing GRB2-like protein 2