ArticleMolecular and cellular biology2003
Gab1 is an integrator of cell death versus cell survival signals in oxidative stress.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 57 citations in OpenAlex.
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- Pancreatic tumor microenvironment reprogramming via alloantigenexpressing virotherapy elicits tumor rejection and improves immunotherapy response.bioRxiv : the preprint server for biology · 2025Article
- The Role of GAB1 in Cancer.Cancers · 2023Review
- S100a8 silencing attenuates inflammation, oxidative stress and apoptosis in BV2 cells induced by oxygen‑glucose deprivation and reoxygenation by upregulating GAB1 expression.Molecular medicine reports · 2021Article
- Pasireotide protects mammalian cochlear hair cells from gentamicin ototoxicity by activating the PI3K-Akt pathway.Cell death & disease · 2019Article
- LIF-dependent survival of embryonic stem cells is regulated by a novel palmitoylated Gab1 signalling protein.Journal of cell science · 2018Article
- Recent advances of adapter proteins in the regulation of heart diseases.Heart failure reviews · 2017Review
- Discovery of a Novel Inhibitor of the Protein Tyrosine Phosphatase Shp2.Scientific reports · 2015Article
- Inhibition of Spleen Tyrosine Kinase Potentiates Paclitaxel-Induced Cytotoxicity in Ovarian Cancer Cells by Stabilizing Microtubules.Cancer cell · 2015Article
- Gab1 Is Modulated by Chronic Hypoxia in Children with Cyanotic Congenital Heart Defect and Its Overexpression Reduces Apoptosis in Rat Neonatal Cardiomyocytes.BioMed research international · 2015Article
- Deletion of 4q28.3-31.23 in the background of multiple malformations with pulmonary hypertension.Molecular cytogenetics · 2014Article
- Protein tyrosine phosphatase-1B regulates the tyrosine phosphorylation of the adapter Grb2-associated binder 1 (Gab1) in the retina.Cell communication and signaling : CCS · 2013Article
- Anti-apoptotic role of caspase-cleaved GAB1 adaptor protein in hepatocyte growth factor/scatter factor-MET receptor protein signaling.The Journal of biological chemistry · 2012Article
- Met receptor tyrosine kinase signals through a cortactin-Gab1 scaffold complex, to mediate invadopodia.Journal of cell science · 2012Article
- Article
- Resolution of infection promotes a state of dormancy and long survival of CD4 memory T cells.Immunology and cell biology · 2011Article
- A systems biology approach identifies molecular networks defining skeletal muscle abnormalities in chronic obstructive pulmonary disease.PLoS computational biology · 2011Article
- Transcriptional analysis implicates endoplasmic reticulum stress in bovine spongiform encephalopathy.PloS one · 2010Article
- Silencing of the JNK pathway maintains progesterone receptor activity in decidualizing human endometrial stromal cells exposed to oxidative stress signals.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- The Src homology 2 domain tyrosine phosphatases SHP-1 and SHP-2: diversified control of cell growth, inflammation, and injury.Histology and histopathology · 2007Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Upon the addition of different growth factors and cytokines, the Gab1 docking protein is tyrosine phosphorylated and in turn activates different signaling pathways. On the basis of the large body of evidence concerning cross talk between the signaling pathways activated by growth factors and oxidative stress, we decided to investigate the role of Gab1 in oxidative injury. We stimulated wild-type mouse embryo fibroblasts (MEF) or MEF with a homozygous deletion of the Gab1 gene (-/- MEF) with H(2)O(2). Our results show that Gab1 is phosphorylated in a dose- and time-dependent manner after H(2)O(2) triggering. Gab1 then recruits molecules such as SHP2, phosphatidylinositol 3-kinase (PI3K), and Shc. Gab1 phosphorylation is sensitive to the Src family kinase inhibitor PP2. Furthermore, we demonstrate that Gab1 is required for H(2)O(2)-induced c-Jun N-terminal kinase (JNK) activation but not for ERK2 or p38 activation. Reconstitution of Gab1 in -/- MEF rescues JNK activation, and we find that this is dependent on the SHP2 binding site in Gab1. Cell viability assays reveal that Gab1 has a dual role in cell survival: a positive one through its interaction with PI3K and a negative one through its interaction with SHP2. This is the first report identifying Gab1 as a component in oxidative stress signaling and one that is required for JNK activation.
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