Browse our anti-SH3G2 (SH3G2) Antibodies

Human Endophilin-A1 (SH3G2) interaction partners

1. endophilin A1 plays a critical role in epilepsy

2. The results suggest that SH3GL2 suppresses migration and invasion behaviors of glioma cells through negatively regulating STAT3/MMP2 signaling.

3. Alix acts in concert with endophilin A to promote clathrin-independent endocytosis of cholera toxin and to regulate cell migration.

4. This study identified a new mitochondria reprogramming pathway influencing breast cancer progression through SH3GL2 and MFN2. These proteins were frequently lost in breast cancer, which was traceable in the circulating exosomes.

5. Endophilin-1 was a direct and functional downstream target of miR-107.

6. Methylation status of SH3GL2 gene was associated with the TNM staging and HPV infection status of vulvar squamous cell carcinoma.

7. Endophilin-1 positively regulated blood-brain barrier permeability via the EGFR-JNK signaling pathway in hCMEC/D3 cells, which would provide an experimental basis for further research on endophilin-1 mediated the opening of blood-brain barrier .

8. these results reveal a novel function of postsynaptic endophilin A1 in spine morphogenesis, stabilization and synaptic function through the regulation of p140Cap

9. Data indicate that the presence of the susceptible G allele in SNP rs1049430 is associated with the inactivation of SH3-domain GRB2-like 2 protein (SH3GL2) and could be used as a prognostic marker of head and neck squamous cell carcinoma (HNSCC).

10. study described that endophilin-1 is expressed in hCMEC/D3 cells where it regulates the permeability of blood-brain barrier by altering the expression of ZO-1 and occludin via the EGFR-ERK1/2 pathway

11. miR-330 negatively regulated the expression of SH3GL2 in GSCs, which promoted the oncogenic progression of GSCs through activating ERK and PI3K/AKT signaling pathways.

12. these findings identify loss of Sh3gl2 as a frequent event in Urothelial carcinoma (UC) development that promotes disease progression.

13. this study suggests a novel mechanism in which Lpd mediates EGFR endocytosis via Mena downstream of endophilin.

14. Overexpression of EGFR in head and neck squamous cell carcinoma is associated with inactivation of SH3GL2 and CDC25A genes.

15. Data suggest that expression of endothelin-1 and vWF (von Willebrand factor) is up-regulated and eNOS (endothelial nitric oxide synthase) activity is increased in radial artery in diabetic patients with coronary artery disease.

16. Our results indicate that SH3GL2 is frequently deleted in NSCLC and regulates cellular growth and invasion by modulating EGFR function.

17. SH3GL2 gene was identified as the target of miR-330. miRNA-330 plays an oncogenic role in human glioblastoma by regulating SH3GL2 gene and might be a new therapeutic target of human glioblastoma.

18. simulations constitute a multi-dimensional exploration of how EGF-dependent EGFR endocytosis and ERK activation are dynamically affected by scaffolds KSR and MP1, co-regulated by Cbl-CIN85 and Endophilin A1

19. SH3GL2 participates in the regulation of apoptosis through the MEK-ERK signal pathway by adjusting EGFR in the laryngeal carcinoma cell line Hep2

20. Alterations of SH3GL2 and CDKN2A loci have a synergistic role in the development of early-onset breast cancer.

Mouse (Murine) Endophilin-A1 (SH3G2) interaction partners

1. endophilin A1 plays a critical role in epilepsy

2. upregulation of EP expression in amyloid-beta peptide (Abeta)-rich environments leads to changes in both long-term potentiation and learning and memory of transgenic animals

3. Alix acts in concert with endophilin A to promote clathrin-independent endocytosis of cholera toxin and to regulate cell migration.

4. Transcriptional analysis of endophilin-A mutant mice, complemented by proteomics, highlighted ataxia- and protein-homeostasis-related genes and revealed upregulation of the E3-ubiquitin ligase FBXO32/atrogin-1 and its transcription factor FOXO3A.

5. these results reveal a novel function of postsynaptic endophilin A1 in spine morphogenesis, stabilization and synaptic function through the regulation of p140Cap

6. retrolinkin is a binding partner of endophilin A1 and that both proteins are required for BDNF-induced dendrite outgrowth

7. Data report that the parkin ubiquitin-like domain binds SH3 domains from endocytic BAR proteins such as endophilin-A with an affinity comparable to proline-rich domains from well-established SH3 partners.

8. Tip-to-tip interactions between the BAR domains in a trigonal crystal form of Snx9(PX-BAR) reminiscent of functionally important interactions described for F-BAR domains.

9. Results sugest that reduced or defective OPHN1 signaling impairs synaptic vesicle cycling at hippocampal synapses.