Ask about this productRelated genes to: Sh3glb1 Blocking Peptide
- Gene:
- SH3GLB1 NIH gene
- Name:
- SH3 domain containing GRB2 like, endophilin B1
- Previous symbol:
- -
- Synonyms:
- CGI-61, KIAA0491, Bif-1, PPP1R70
- Chromosome:
- 1p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2017-02-21
Related products to: Sh3glb1 Blocking Peptide
Related articles to: Sh3glb1 Blocking Peptide
- - Source: PubMed
Publication date: 2026/05/11
Gao AnboZou JinMao ZhenjiangZhou HongZeng Gaofeng - Autophagy involves the rapid growth of phagophores through membrane addition. This growth is triggered by vesicles containing the Atg9A protein. However, Atg9A is not incorporated into mature autophagosomes. We now demonstrate that Dynamin-2 (Dnm2) colocalizes with the BAR domain protein Endophilin-B1 (EndoB1/Bif-1/SH3GLB1) and other autophagy proteins when autophagy is induced. Our data suggest that Atg9A is retrieved from phagophores via fission, with Dnm2 acting as the membrane scission protein. Blocking Atg9A recycling, either by mutating Dnm2, using RNA interference, or applying chemical inhibitors, results in Atg9A remaining in autophagosomes and being degraded during autophagy. Overall, these findings provide new insights into the roles of membrane-scission proteins in autophagy. - Source: PubMed
Publication date: 2026/03/13
Caliri AndrewRiera Alejandro MartorellSaha AkashKolitsida PanagiotaMartinez Cinta IriondoItskanov SamuelSteffen JanosKoehler Carla Mvan der Bliek Alexander M - Acute lung injury (ALI) accompanied by an inflammatory response is an important complication after drowning. Macrophage activation and polarization are implicated in the inflammatory process of lipopolysaccharide (LPS)‑induced ALI (LPS‑ALI), but little is known about drowning‑induced ALI (drowning‑ALI). SH3 domain‑containing GRB2‑like protein B1 (SH3GLB1) is a member of the endophilin family and has been shown to be involved in mitochondrial morphological changes and autophagy. However, its role in ALI remains unclear. Thus, the present study aimed to examine the effects of macrophages in drowning‑ALI and to elucidate the underlying molecular mechanism involved. In the present study, single‑cell RNA‑sequencing indicated that the regulation of macrophages in drowning‑ALI was similar to that in LPS‑ALI by single‑cell profiling of lung immune cells isolated from the lungs. Specifically, SH3GLB1 was highly expressed in macrophages of drowning‑ALI mouse models and was related to inflammation. Furthermore, SH3GLB1 deletion ameliorated LPS‑ALI or drowning‑ALI. By contrast, the restoration of SH3GLB1 expression provoked LPS‑ALI and drowning‑ALI. Mechanistically, SH3GLB1 was shown to interact with Rab7 to contribute to mitophagy, which resulted in mitochondrial dysfunction. Overall, these findings indicated that SH3GLB1 is required for Rab7‑mediated mitophagy in inflammation during ALI and could be a novel target for lung protection. - Source: PubMed
Publication date: 2026/03/27
Ning HongjuanDeng JingyuGao YonghengZhang WeiChen JianGuo XianJin Faguang - To explore transcriptome differences between diploid and aneuploidy embryos, identify non-invasive screening targets for aneuploidy embryos, and establish a theoretical basis for a pathogenic model. - Source: PubMed
Publication date: 2026/03/23
Duan RubingLiang XiaodongYang YingGuo Jianghua - Glioblastoma (GBM) is a prevalent malignant brain tumor prone to drug resistance. We previously found a strong correlation between SH3 domain GRB2-like endophilin B1 (SH3GLB1) and superoxide dismutase 2 (SOD2), which converts O to hydrogen peroxide (HO). Prior studies show that HO redox signaling is vital for physiological processes and can drive tumor progression. Therefore, we aim to define how HO signaling regulates SH3GLB1 and AKT (protein kinase B) pathways in GBM and to assess whether modulating HO reverses temozolomide (TMZ) resistance. - Source: PubMed
Publication date: 2026/01/19
Hsueh Wei-TingChang Kwang-YuTsai Chin-ChuanChen Kuan-TsoTsai Kuen-JangHong Zi-XuanLiu Chan-ChuanChu Jui-MeiQiu Li-YingLan Yu-YanChien Chia-Hung