NCK, an SH2- and SH3 domain-containing protein, becomes phosphorylated and associated with tyrosine kinase receptors upon growth factor stimulation. The sequence of NCK suggests that NCK functions as a linker between receptors and a downstream signaling molecule. To determine if NCK can mediate growth factor-stimulated responses, we measured the ability of NCK to activate the fos promoter. We found that in NIH 3T3 cells, NCK strongly activates this promoter. The effect of NCK on the fos promoter is enhanced by c-ras and blocked by dominant negative ras. We also found that NCK binds directly to the guanine nucleotide exchange factor SOS. This interaction is mediated by the SH3 domains of NCK. These findings suggest that NCK can regulate p21ras-dependent gene transcription through interaction with SOS protein.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC230339 | PMC |
| http://dx.doi.org/10.1128/MCB.15.3.1169 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Identifying disulfidptosis-related biomarkers in epilepsy based on integrated bioinformatics and experimental analyses.
Neurobiol Dis
February 2025
Department of Neurology, the First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, Nanning, Guangxi, China. Electronic address:
One of the underlying mechanisms of epilepsy (EP), a brain disease characterized by recurrent seizures, is considered to be cell death. Disulfidptosis, a proposed novel cell death mechanism, is thought to play a part in the pathogenesis of epilepsy, but the exact role is unclear. The gene expression omnibus series (GSE) 33000 and GSE63808 datasets were used to search for differentially expressed disulfidptosis-related molecules (DE-DRMs).
View Article and Find Full Text PDFAllosteric Changes Underlie the Outside-In Transmission of Activatory Signals in the TCR.
Immunol Rev
January 2025
Signaling Research Centers BIOSS and CIBSS, University of Freiburg, Freiburg, Germany.
Rather than being contained in a single polypeptide, and unlike receptor tyrosine kinases, the T cell receptor (TCR) divides its signaling functions among its subunits: TCRα/β bind the extracellular ligand, an antigenic peptide-MHC complex (pMHC), and the CD3 subunits (CD3γ, CD3δ, CD3ε, and CD3ζ) transmit this information to the cytoplasm. How information about the quality of pMHC binding outside is transmitted to the cytoplasm remains a matter of debate. In this review, we compile data generated using a wide variety of experimental systems indicating that TCR engagement by an appropriate pMHC triggers allosteric changes transmitted from the ligand-binding loops in the TCRα and TCRβ subunits to the cytoplasmic tails of the CD3 subunits.
View Article and Find Full Text PDFRecurrent Jaundice Unraveled: A Case of Benign Recurrent Intrahepatic Cholestasis (BRIC) in an Indian Patient.
Cureus
November 2024
General Medicine, Felix Hospital, Noida, IND.
Benign recurrent intrahepatic cholestasis (BRIC) is a rare, autosomal recessive liver disorder characterized by intermittent episodes of cholestasis without progression to chronic liver disease or cirrhosis. Patients experience recurrent jaundice and severe pruritus, significantly impacting their quality of life. This case report presents a 15-year-old boy with a history of recurrent jaundice and pruritus.
View Article and Find Full Text PDFTNIK: A redox sensor in endothelial cell permeability.
Sci Adv
December 2024
School of Cardiovascular and Metabolic Medicine and Sciences, James Black Centre, BHF Centre of Research Excellence, 125 Coldharbour Lane, King's College London, London SE5 9NU, UK.
Dysregulation of endothelial barrier integrity can lead to vascular leak and potentially fatal oedema. TNF-α controls endothelial permeability during inflammation and requires the actin organizing Ezrin-Radixin-Moesin (ERM) proteins. We identified TRAF2 and NCK-interacting kinase (TNIK) as a kinase directly phosphorylating and activating ERM, specifically at the plasma membrane of primary human endothelial cells.
View Article and Find Full Text PDFMolecular basis of the CYFIP2 and NCKAP1 autism-linked variants in the WAVE regulatory complex.
Protein Sci
January 2025
Computational Biomedicine, Institute of Advanced Simulation IAS-5 and Institute of Neuroscience and Medicine INM-9, Forschungszentrum Jülich GmbH, Jülich, Germany.
The WAVE regulatory pentameric complex regulates actin remodeling. Two components of it (CYFIP2 and NCKAP1) are encoded by genes whose genetic mutations increase the risk for autism spectrum disorder (ASD) and related neurodevelopmental disorders. Here, we use a newly developed computational protocol and hotspot analysis to uncover the functional impact of these mutations at the interface of the correct isoforms of the two proteins into the complex.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!