| The SH3 binding site in front of the WH1 domain contributes to the membrane binding of the BAR domain protein endophilin A2. | The SH3 binding site in front of the WH1 domain contributes to the membrane binding of the BAR domain protein endophilin A2.
Sim PF, Chek MF, Nguyen NTH, Nishimura T, Inaba T, Hakoshima T, Suetsugu S. | 01/9/2024 |
| Endophilin A2 regulates B-cell endocytosis and is required for germinal center and humoral responses. | Endophilin A2 regulates B-cell endocytosis and is required for germinal center and humoral responses.
Malinova D, Wasim L, Newman R, Martínez-Riaño A, Engels N, Tolar P., Free PMC Article | 10/30/2021 |
| EV71 enters Caco-2 cells mainly via an endophilin-A2-mediated endocytic pathway. | Endophilin-A2-mediated endocytic pathway is critical for enterovirus 71 entry into caco-2 cells.
Chen SL, Liu YG, Zhou YT, Zhao P, Ren H, Xiao M, Zhu YZ, Qi ZT., Free PMC Article | 09/7/2019 |
| FBP17 and CIP4 prime the membrane of resting cells for fast endophilin-mediated endocytosis by recruiting the 5'-lipid phosphatase SHIP2 and lamellipodin to mediate the local production of phosphatidylinositol-3,4-bisphosphate and endophilin pre-enrichment. | FBP17 and CIP4 recruit SHIP2 and lamellipodin to prime the plasma membrane for fast endophilin-mediated endocytosis.
Chan Wah Hak L, Khan S, Di Meglio I, Law AL, Lucken-Ardjomande Häsler S, Quintaneiro LM, Ferreira APA, Krause M, McMahon HT, Boucrot E., Free PMC Article | 05/11/2019 |
| Study observed elevated EA2 gene expression in the subcutaneous compared to that in the visceral human adipose tissue. EA2 gene expression negatively correlated with adiponectin and chemerin in visceral adipose tissue, and positively correlated with TNF-alpha in subcutaneous adipose tissue. EA2 gene expression was significantly downregulated during differentiation of preadipocytes in vitro. | Endophilin A2: A Potential Link to Adiposity and Beyond.
Alfadda AA, Sallam RM, Gul R, Hwang I, Ka S., Free PMC Article | 07/14/2018 |
| Our study provides novel evidence of Endo II function in HER2+ cancer cell motility and trafficking of HER2 that relates to effective treatments with trastuzumab or T-DM1. Thus, differential expression of Endo II may relate to sensitivity or resistance to trastuzumab-based therapies for HER2+ cancers | Endophilin A2 promotes HER2 internalization and sensitivity to trastuzumab-based therapy in HER2-positive breast cancers.
Baldassarre T, Truesdell P, Craig AW., Free PMC Article | 06/9/2018 |
| Expression level of SH3GL1 was widely upregulated in human OS tissues, and their overexpression was significantly correlated with more aggressive clinicopathological features. | Essential role of SH3GL1 in interleukin-6(IL-6)- and vascular endothelial growth factor (VEGF)-triggered p130(cas)-mediated proliferation and migration of osteosarcoma cells.
Li EQ, Zhang JL. | 03/3/2018 |
| 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 | Endophilin-A2-mediated increase in scavenger receptor expression contributes to macrophage-derived foam cell formation.
Huang EW, Liu CZ, Liang SJ, Zhang Z, Lv XF, Liu J, Zhou JG, Tang YB, Guan YY. | 12/23/2017 |
| inhibition of SH3GL1 reverses multidrug resistance through declining P-glycoprotein expression via the EGFR/ERK/AP-1 pathway. | SH3GL1 inhibition reverses multidrug resistance in colorectal cancer cells by downregulation of MDR1/P-glycoprotein via EGFR/ERK/AP-1 pathway.
Guan H, Zhao P, Dai Z, Liu X, Wang X. | 02/18/2017 |
| Endo II expression was highest in triple-negative breast cancers tumors compared with other subtypes, and at the level of gene expression, high Endo II was associated with reduced relapse-free survival in patients with basal-like breast cancers. | Endophilin A2 Promotes TNBC Cell Invasion and Tumor Metastasis.
Baldassarre T, Watt K, Truesdell P, Meens J, Schneider MM, Sengupta SK, Craig AW. | 03/19/2016 |
| results establish a novel function of endoA2 in clathrin-independent endocytosis | Endophilin-A2 functions in membrane scission in clathrin-independent endocytosis.
Renard HF, Simunovic M, Lemière J, Boucrot E, Garcia-Castillo MD, Arumugam S, Chambon V, Lamaze C, Wunder C, Kenworthy AK, Schmidt AA, McMahon HT, Sykes C, Bassereau P, Johannes L., Free PMC Article | 02/14/2015 |
| 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. | EEN regulates the proliferation and survival of multiple myeloma cells by potentiating IGF-1 secretion.
Huang EW, Xue SJ, Li XY, Xu SW, Cheng JD, Zheng JX, Shi H, Lv GL, Li ZG, Li Y, Liu CH, Chen XH, Liu H, Li J, Liu C. | 07/26/2014 |
| MIR218 functions as a tumor suppressor by regulating SH3GL1 expression in medulloblastoma cancer cells. | miR-218 is downregulated and directly targets SH3GL1 in childhood medulloblastoma.
Shi J, Yang L, Wang T, Zhang J, Guo X, Huo X, Niu H. | 03/22/2014 |
| SH3GL1 may be involved in the oncogenic process of gliomas and effectively elicit an autologous antibody response in low-grade gliomas. | Autologous antibody to src-homology 3-domain GRB2-like 1 specifically increases in the sera of patients with low-grade gliomas.
Matsutani T, Hiwasa T, Takiguchi M, Oide T, Kunimatsu M, Saeki N, Iwadate Y., Free PMC Article | 06/29/2013 |
| Two endophilin A2 mutants, E264A and E264R, have different effects on how endophilin interacts with other proteins, such as dynamin or beta1-adrenergic receptors. | Characterization of two distinct modes of endophilin in clathrin-mediated endocytosis.
Zhang J, Fan J, Tian Q, Song Z, Zhang JF, Chen Y. | 01/12/2013 |
| Idiopathic scoliosis is a multifactorial genetic disease and SH3GL1 may be one of the pathogenic genes for this disease. | Epidemiological survey of idiopathic scoliosis and sequence alignment analysis of multiple candidate genes.
Yang T, Jia Q, Guo H, Xu J, Bai Y, Yang K, Luo F, Zhang Z, Hou T., Free PMC Article | 09/22/2012 |
| A protein encoded by this locus was found to be differentially expressed in postmortem brains from patients with atypical frontotemporal lobar degeneration. | Proteomic analysis identifies dysfunction in cellular transport, energy, and protein metabolism in different brain regions of atypical frontotemporal lobar degeneration.
Martins-de-Souza D, Guest PC, Mann DM, Roeber S, Rahmoune H, Bauder C, Kretzschmar H, Volk B, Baborie A, Bahn S. | 04/26/2012 |
| SH3GL1 is possibly one of the disease associated genes of adolescent idiopathic scoliosis. | [Comparative analysis of sequence alignment of SH3GL1 gene as a disease candidate gene of adolescent idiopathic scoliosis].
Yang T, Xu JZ, Jia QZ, Guo H, Luo F, Ye Q, Bai Y. | 03/26/2011 |
| findings reveal a concomitant activation of endocytosis and ERK signaling by BPGAP1 via the coupling of its proline-rich region, which targets EEN and its functional GAP domain | Activation of EGF receptor endocytosis and ERK1/2 signaling by BPGAP1 requires direct interaction with EEN/endophilin II and a functional RhoGAP domain.
Lua BL, Low BC. | 01/21/2010 |
| Our results suggest that distinct subcellular localization of the endophilin A family members probably underpins their diverse cellular functions and indicates a role for EEN/EA2 in the cell cycle. | Subcellular localization of EEN/endophilin A2, a fusion partner gene in leukaemia.
Cheung N, So CW, Yam JW, So CK, Poon RY, Jin DY, Chan LC., Free PMC Article | 01/21/2010 |
| new mechanism for MLL-EEN-mediated leukemogenesis in which MLL-EEN interferes with the Ras-suppressing activities of EBP through direct interaction. | Identification and characterization of EBP, a novel EEN binding protein that inhibits Ras signaling and is recruited into the nucleus by the MLL-EEN fusion protein.
Yam JW, Jin DY, So CW, Chan LC. | 01/21/2010 |
| EEN part plays an essential role in leukemogenesis caused by MLL-EEN. | Functional contribution of EEN to leukemogenic transformation by MLL-EEN fusion protein.
Liu H, Chen B, Xiong H, Huang QH, Zhang QH, Wang ZG, Li BL, Chen Z, Chen SJ. | 01/21/2010 |