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Human Monoclonal SH2D2A Primary Antibody für FACS, IF - ABIN2731957
Pandya, Leergaard, Dissen, Haraldsen, Spurkland: Expression of the T cell-specific adapter protein in human tissues. in Scandinavian journal of immunology 2014
Data indicate that the T cell-specific adaptor protein (TSAd) SH2 domain interacts with CD6 antigen and linker for activation of T cells protein (LAT) phosphotyrosine (pTyr) peptides.
TSAD binds to and co-localizes with Nck. Expression of TSAD increases both Nck-Lck and Nck-SLP-76 interaction in T cells.
The kinase Itk and the adaptor TSAd change the specificity of the kinase Lck in T cells by promoting the phosphorylation of Tyr192.
Data indicate the expression pattern of T cell-specific adapter protein (TSAd) in various healthy lymphoid and non-lymphoid tissues.
in chronic inflammatory demyelinating polyneuropathy we found an association with a homozygous genotype for a low repeat number of tandem GA in the SH2D2A gene
TSAd, through its interaction with both Itk and Lck, primes Itk for Lck mediated phosphorylation and thereby regulates CXCL12 induced T cell migration and actin cytoskeleton rearrangements
TSAd associates with laminin binding protein and mediates T lymphocyte migration during T cell activation
'short' alleles of the promoter could contribute to the genetic susceptibility to Juvenile Rheumatoid Arthritis
TSAd appears to contribute to interleukin-2 synthesis at multiple different levels
upon chemokine stimulation, Lad acts as an adaptor protein that links the G protein beta subunit to the tyrosine kinases Lck and Zap-70, thereby mediating T-cell migration
SH2D2A expression is regulated both at the transcriptional and translational level.
This study found a significant association between CIDP and the genotype GA13-16 homozygote (OR 3.167; p 0.013).
lymphocyte-specific protein tyrosine kinase binds to T cell-specific adapter protein (TSAd) prolines and phosphorylates and interacts with the three C-terminal TSAd tyrosines
the present study shows that the SH2D2A gene may contribute to susceptibility to MS.
These results revealed that vascular sprouting and permeability are both controlled through the VEGFR2-TSAd-c-Src signaling pathway in a subset of tissues, which may be useful in developing strategies to control tissue-specific pathological angiogenesis.
Sh2d2a protein deficient mice display reduced clearance of Dm157 MCMV infection in the spleen.
Results suggest a modulatory role for T cell specific adapter protein SH2D2A in T cell mediated immune surveillance of cancer.
Data show that tyrosine phosphorylation of VEGF receptor 2 (VEGFR2) facilitates binding of VEGFR2 to the Rous sarcoma (Src) homology 2-domain of T cell-specific adaptor (TSAd), which in turn regulates VEGF-induced activation of the c-Src tyrosine kinase.
results show that TSAd, particularly the SH2 domain of TSAd, is essential for the effector functions of T cells.
role of TSAd as a critical regulator of T cell death whose absence promotes systemic autoimmunity
The major role of T cell-specific adapter protein in peripheral T cell cytoplasm is for activation of LCK protein tyrosine kinase at the outset of T cell receptor signal transduction
Although Rlk/Itk-binding protein (RIBP) is coexpressed with related adaptor lymphocytes of unknown function X (ALX) protein on both T- and B-lymphocytes during cell development, no redundancy or synergy is found.
This gene encodes an adaptor protein thought to function in T-cell signal transduction. A related protein in mouse is responsible for the activation of lymphocyte-specific protein-tyrosine kinase and functions in downstream signaling. Alternative splicing results in multiple transcript variants.
SH2 domain protein 2A
, SH2 domain-containing protein 2A
, T cell specific adapter protein TSAd
, T lymphocyte specific adaptor protein
, VEGF receptor-associated protein
, Lck-associated adapter protein
, Rlk/Itk-binding protein
, T cell-specific adapter protein
, p56Lck-associated adapter protein