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Joseph Lin

Researcher at Sonoma State University

Publications -  51
Citations -  3520

Joseph Lin is an academic researcher from Sonoma State University. The author has contributed to research in topics: Signal transduction & T-cell receptor. The author has an hindex of 25, co-authored 47 publications receiving 3084 citations. Previous affiliations of Joseph Lin include Washington University in St. Louis & University of California, San Francisco.

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Signal transduction by the TCR for antigen.

TL;DR: The past several years have seen the beginning of a shift in the way that TCR signal transduction is studied, with the identification of distinct formations of signaling molecules at junctions between T cells and antigen-presenting cells, the role of the cytoskeleton and the partitioning of molecules into specialized lipid subdomains being the subjects of many publications.
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Redox chemistry and chemical biology of H2S, hydropersulfides, and derived species: implications of their possible biological activity and utility.

TL;DR: The basic chemical biology of H2S as well as other related or derived species is discussed and reviewed, and this review particularly focuses on the per- and polysulfides which are likely in equilibrium with free H 2S and which may be important biological effectors themselves.
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Regulation of the Pancreatic Pro-Endocrine Gene Neurogenin3

TL;DR: A model in which the ngn3 gene is activated by the coordinated activities of several pancreatic transcription factors and inhibited by Notch signaling through HES1 is suggested, which suggests that the addition of distal sequences greatly enhances transgene expression.
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T cell receptor signalling.

TL;DR: Upon engagement of the TCR by antigen presented on major histocompatibility complex (MHC) molecules, the Src family kinase Lck is activated and proceeds to phosphorylate immunoreceptor tyrosine-based activation motifs (ITAMs) on the e, δ, γ and ζ subunits of theTCR.
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It's all Rel-ative: NF-κB and CD28 costimulation of T-cell activation

TL;DR: Several lines of evidence indicate that the nuclear factor (NF)-kappaB pathway is perhaps the most relevant biochemical or transcriptional target for the costimulatory activity of CD28.