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The Src family kinases possess two sites of tyrosine phosphorylation that are critical to the regulation of kinase activity. Autophosphorylation on an activation loop tyrosine residue (Tyr 416 in commonly used chicken c-Src numbering) increases catalytic activity, while phosphorylation of a C-terminal tyrosine (Tyr 527 in c-Src) inhibits activity. The latter modification is achieved by the tyrosine kinase Csk (C-terminal Src Kinase), but the complete inactivation of the Src family kinases also requires the dephosphorylation of the activation loop tyrosine. The SH3 domain of Csk recruits the tyrosine phosphatase PEP, allowing for the coordinated inhibition of Src family kinase activity. We have discovered that Csk forms homodimers through interactions mediated by the SH3 domain in a manner that buries the recognition surface for SH3 ligands. The formation of this dimer would therefore block the recruitment of tyrosine phosphatases and may have important implications for the regulation of Src kinase activity.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2766628 | PMC |
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0007683 | PLOS |
Life Sci Alliance
May 2025
https://ror.org/021018s57 Biomolecular NMR Laboratory, Department of Inorganic and Organic Chemistry, Universitat de Barcelona (UB), Barcelona, Spain
Src tyrosine kinase regulates cell growth and adhesion through membrane signaling, and its deregulation is associated with cancer. Although active Src is anchored to the plasma membrane, the role of membrane lipids in its regulation remains unclear. Here, we report that Src self-associates via a lysine cluster in its SH4 region, a process mediated by lipids in human cells and in vitro.
View Article and Find Full Text PDFActas Esp Psiquiatr
March 2025
Department of Pediatric, The First People's Hospital of Taizhou, 318020 Taizhou, Zhejiang, China.
Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social communication and limited behavior. Despite the association of numerous synaptic gene mutations with ASD, the presence of behavioral abnormalities in mice expressing autism-associated R617W mutation in synaptic adhesion protein neuroligin-3 (NL3) has not been established. This work focuses on establishing a mouse model of ASD caused by NL3 R617W missense mutation (NL3R617W) and characterizing and profiling the molecular as well as behavioral features of the animal model.
View Article and Find Full Text PDFNat Commun
March 2025
Department of Pediatrics, Division of Hematology & Oncology, Children's Mercy Research Institute, Kansas City, MO, USA.
Missense mutations in the TP53 (p53) gene have been linked to malignant progression. However, our in-silico analyses reveal that hepatocellular carcinoma (HCC) patients with mutant p53 (mutp53) have better overall survival compared to those with p53-null (p53) HCC, unlike other cancer types. Given the historical use of sorafenib (SOR) monotherapy for advanced HCC, we hypothesize that mutp53 increases sensitivity to SOR, a multikinase inhibitor that induces endoplasmic reticulum (ER) stress.
View Article and Find Full Text PDFFront Immunol
March 2025
Department of Biological Sciences, DePaul University, Chicago, IL, United States.
The bursa of Fabricius has been a durable model of B lymphocyte development. Yet there are unique aspects of B- lymphocyte development in the bursa that remain to be elucidated, and these may reveal important functional differences in the avian system and distinct evolutionary mechanisms from the canonical murine and human models of B- lymphocyte development. Our laboratory has been interested in the function of the chB6 alloantigen.
View Article and Find Full Text PDFCancer Res
March 2025
University of Helsinki, Helsinki, Finland.
Engineered T cell therapies have emerged as a promising approach for cancer treatment, yet their application to solid tumors remains challenging due to the limited specificity and persistence of current antigen recognition strategies. Here, we introduced sherpabodies, engineered from a human SH3 domain scaffold, as a class of antibody-mimetic proteins capable of precise tumor-associated antigen recognition. A phage display library identified sherpabodies against a panel of popular tumor-associated antigens (TAA), which were subsequently incorporated into second-generation chimeric antigen receptor constructs that were termed sherpabody-guided CARs (SbCARs).
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