Magic™ Anti-LCK (Phospho Y393) polyclonal antibody

Name: Magic™ Anti-LCK (Phospho Y393) polyclonal antibody
SKU: DPABH-01413
Rating: 5 (1 reviews)

Rabbit Anti-Human LCK (Phospho Y393) polyclonal antibody for WB

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COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Human

Immunogen

Synthetic phospho-peptide against an internal region around Y393 of the Human Lck protein.

Conjugate

Unconjugated

Applications

Application Notes

WB: 1/500 - 1/1000

Target

Alternative Names

LCK; lymphocyte-specific protein tyrosine kinase; LSK; YT16; IMD22; p56lck; pp58lck; tyrosine-protein kinase Lck; leukocyte C-terminal Src kinase; p56(LSTRA) protein-tyrosine kinase; t cell-specific protein-tyrosine kinase; proto-oncogene tyrosine-protein

Entrez Gene ID

2322

UniProt ID

P36888

Product Background

Antigen Description

Tyrosine kinase that plays an essential role for the selection and maturation of developing T-cell in the thymus and in mature T-cell function. Is constitutively associated with the cytoplasmic portions of the CD4 and CD8 surface receptors and plays a key role in T-cell antigen receptor(TCR)-linked signal transduction pathways. Association of the TCR with a peptide antigen-bound MHC complex facilitates the interaction of CD4 and CD8 with MHC class II and class I molecules, respectively, and thereby recruits the associated LCK to the vicinity of the TCR/CD3 complex. LCK then phosphorylates tyrosines residues within the immunoreceptor tyrosines-based activation motifs (ITAMs) in the cytoplasmic tails of the TCRgamma chains and CD3 subunits, initiating the TCR/CD3 signaling pathway. In addition, contributes to signaling by other receptor molecules. Associates directly with the cytoplasmic tail of CD2, and upon engagement of the CD2 molecule, LCK undergoes hyperphosphorylation and activation. Also plays a role in the IL2 receptor-linked signaling pathway that controls T-cell proliferative response. Binding of IL2 to its receptor results in increased activity of LCK. Is expressed at all stages of thymocyte development and is required for the regulation of maturation events that are governed by both pre-TCR and mature alpha beta TCR. Phosphorylates RUNX3.

Pathway

Adaptive Immune System; Atypical NF-kappaB pathway; CD28 co-stimulation; CD28 dependent Vav1 pathway

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

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Customer Reviews

References

The ligands of translocator protein inhibit human Th1 responses and the rejection of murine skin allografts

CLINICAL SCIENCE

Authors: Zhang, Yannan; Yu, Sifei; Li, Xiaomin; Yang, Binyan; Wu, Changyou

Abstract

The translocator protein (TSPO) ligands affected inflammatory and immune responses. However, the exact effects of TSPO ligands on Th1 responses in vitro and in vivo are still unclear. In the present study, we found that TSPO ligands, FGIN1-27 and Ro5-4864, suppressed the cytokine production in a dose-dependent manner by purified human CD4(+) T-cells from peripheral blood mononuclear cells (PBMCs) after stimulation. TSPO ligands inhibited the production of interferon gamma (IFN-gamma) by memory CD4+ T-cells and the differentiation of naive CD4+ T-cells into Th1 cells via suppressing the activity of the corresponding transcription factors as indicated by reduced expression of T-bet and down-regulation of STAT1, STAT4 and STAT5 phosphorylation. TSPO ligands suppressed cell proliferation and activation of CD4+ T-cells by the inhibition of TCR signal transduction including membrane proteins: Zap, Lck, Src; cytoplasm proteins: Plc gamma 1, Slp-76, ERK, JNK and the nucleoproteins: c-Jun and c-Fos. In addition, FGIN1-27 inhibited mixed lymphocyte reactions by human or murine cells. After the transplantation of allogeneic murine skin, injection of FGIN1-27 into mice prevented graft rejection by inhibition of cell infiltration and IFN-gamma production. Taken together, our data suggest that TSPO ligands inhibit Th1 cell responses and might be novel therapeutic medicine for the treatment of autoimmune diseases and prevention of transplant rejection.

Low level of Lck kinase in Th2 cells limits expression of CD4 co-receptor and S73 phosphorylation of transcription factor c-Jun

SCIENTIFIC REPORTS

Authors: Shebzukhov, Yury V.; Stanislawiak, Silke; Bezhaeva, Taisiya R.; Nedospasov, Sergei A.; Kuprash, Dmitry V.

Abstract

The Src-family tyrosine kinase Lck is an enzyme associated with the CD4 and CD8 co-receptors and promoting signaling through the T cell receptor (TCR) complex. The levels of Lck expression and activity change during the development and differentiation of T cells. Here we show that Lck expression is higher in Th1 cells as compared to Th2 cells. Ectopic overexpression of Lck in Th2 cells results in increased expression of CD4 co-receptor and enhanced S73 phosphorylation of transcription factor c-Jun. Our findings indicate that TCR-mediated signaling in Th2 cells may be directly attenuated by Lck protein expression level.