Results 1 to 10 of about 17,555 (209)

Delayed onset of positive feedback activation of Rab5 by Rabex-5 and Rabaptin-5 in endocytosis. [PDF]

open access: yesPLoS ONE, 2010
Rabex-5 is a guanine nucleotide exchange factor (GEF) that specifically activates Rab5, i.e., converting Rab5-GDP to Rab5-GTP, through two distinct pathways to promote endosome fusion and endocytosis.
Huaiping Zhu, Hong Qian, Guangpu Li
doaj   +2 more sources

Structure-Based Discovery of Neoandrographolide as a Novel Inhibitor of Rab5 to Suppress Cancer Growth

open access: yesComputational and Structural Biotechnology Journal, 2020
Rab5 is a small GTPase that plays a crucial role in oncogenic signal transduction, which was considered as an attractive target for cancer therapy. Rapid GDP/GTP exchange in the packet of Rab5 sustains its high activity for promoting cancer progression ...
Yang Wang, Qing-Yu He, Run-Dong Fang
exaly   +3 more sources

A novel RAB5 binding site in human VPS34-CII that is likely the primordial site in eukaryotic evolution [PDF]

open access: yeseLife
RAB5-GTP activation of the multiprotein VPS34 complex II (VPS34-CII) is critical for endosomal sorting and maturation, phagocytosis, and receptor downregulation.
Saule Spokaite   +4 more
doaj   +2 more sources

Helicobacter pylori infection activates the HIF-1α/ALS2/Rab5 signaling axis in gastric cells [PDF]

open access: yesCell Communication and Signaling
Helicobacter pylori (H. pylori) infection has been associated with gastric carcinogenesis by activating different signaling pathways. In gastric cancer cells, H.
Daniela Herrera-Ramírez   +12 more
doaj   +2 more sources

Preformed fibrils of α-synuclein rapidly activate LRRK2 on early endosomes, driving Rab5 phosphorylation and disrupting endolysosomal and synaptic function [PDF]

open access: yesnpj Parkinson's Disease
Parkinson’s disease (PD) is characterized by α-synuclein aggregation and perturbation of the endolysosomal network (ELN), yet the molecular mechanisms linking α-synuclein pathology to neuronal dysfunction remain unclear.
Xinxin Zuo   +8 more
doaj   +2 more sources

Rab GTPases drive ligand‐independent NOTCH1 activation via altered endocytic trafficking in chronic lymphocytic leukemia [PDF]

open access: yesHemaSphere
Clinically relevant NOTCH1 activation is frequently observed in chronic lymphocytic leukemia (CLL), even in the absence of gene mutations, raising questions about the underlying mechanisms.
Filomena De Falco   +17 more
doaj   +2 more sources

Lipid turnover and GEF recruitment collectively determine Rab5 recruitment and activation during the first step of early endosome formation [PDF]

open access: yesNature Communications
Early endosomes are the pivotal sorting station in eukaryotic cells. A longstanding critical question is how the small GTPase Rab5 is precisely targeted to the correct membrane to initiate early endosome formation.
Yongtao Du   +12 more
doaj   +2 more sources

Vinculin and Rab5 complex is required [correction of requited]for uptake of Staphylococcus aureus and interleukin-6 expression. [PDF]

open access: yesPLoS ONE, 2014
Vinculin, a 116-kDa membrane cytoskeletal protein, is an important molecule for cell adhesion; however, little is known about its other cellular functions.
Makoto Hagiwara   +12 more
doaj   +1 more source

Role of Rab5 in the formation of macrophage-derived foam cell

open access: yesLipids in Health and Disease, 2017
Background Foam cells play a key role in the occurrence and pathogenesis of atherosclerosis. Its formation starts with the ingestion of oxidized low-density lipoprotein (oxLDL).
Lokwern Chan   +7 more
doaj   +1 more source

Dynamin- and Rab5-dependent endocytosis of a Ca2+ -activated K+ channel, KCa2.3. [PDF]

open access: yesPLoS ONE, 2012
Regulation of the number of ion channels at the plasma membrane is a critical component of the physiological response. We recently demonstrated that the Ca(2+)-activated K(+) channel, KCa2.3 is rapidly endocytosed and enters a Rab35- and EPI64C-dependent
Yajuan Gao   +4 more
doaj   +1 more source

Home - About - Disclaimer - Privacy