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Elevated expression of Lnk in polycystic ovary syndrome suggests that Lnk probably plays a role in the development of insulin (show INS ELISA Kits) resistance.
Hypercholesterolemia acts in platelets and hematopoietic progenitors to exacerbate thrombosis and atherosclerosis associated with SH2B3 deficiency.
The polymorphisms in LNK gene correlated to the clinical type of myeloproliferative neoplasms regardless of the JAK2 (show JAK2 ELISA Kits) polymorphism.
SH2B3 mutations occur infrequently, and exon 8 in SH2B3 may be the most frequent mutational area in BCR-ABL (show ABL1 ELISA Kits) negative myeloproliferative neoplasms patients in Korea.
LNK/SH2B3 is a key driver gene for human hypertension, and alteration of LNK in animal models has a profound effect on inflammation and hypertension. Thus, LNK is a potential therapeutic target for this disease and its devastating consequences.
Meta-analysis of genome-wide association studies identifies common susceptibility polymorphisms for colorectal and endometrial cancer near SH2B3 and TSHZ1 (show TSHZ1 ELISA Kits).
results suggest that LNK suppresses IL-7R/JAK (show JAK3 ELISA Kits)/STAT (show STAT1 ELISA Kits) signaling to restrict pro-/pre-B progenitor expansion and leukemia development, providing a pathogenic mechanism and a potential therapeutic approach for B-ALLs with LNK mutations.
the minor allele A of rs3184504 (A vs G, OR = 1.18, 95%CI = 1.12-1.24, P < 0.001) in SH2B3 significantly increased celiac disease susceptibility (Meta-Analysis)
A number of mutations in LNK have been described in a variety of myeloproliferative neoplasms some of which have been demonstrated to cause increased cellular proliferation.
The single-nucleotide polymorphism in SH2B3 was significantly associated with Hypertension in an Algerian population sample.
The LNK plays a regulatory role in the palmitate-related preadipocyte apoptosis and might be involved in adipose tissue dysfunction.
We found that a significant number of genes predicted to be regulated by SH2B3 in gene networks are perturbed in Sh2b3(-/-) mice, which demonstrate an exaggerated pressor response to angiotensin II infusion.
SH2B3 functions as a novel and effective modulator of cardiac remodeling and failure.
Loss of LNK in hematopoietic cells is primarily responsible for the observed renal and vascular inflammation and predisposition to hypertension.
Lnk/Sh2b3 plays a regulatory role in the expansion of Dendritic cells and might influence inflammatory immune responses in peripheral lymphoid tissues.
results reveal a link between Lnk and immune cell-mediated intestinal tissue destruction.
IL-11 (show IL11 ELISA Kits) therefore drives a pathway that enhances HSPC (show PSMA7 ELISA Kits) radioresistance and radiation-induced B-cell malignancies, but is normally attenuated by the inhibitory adaptor Lnk.
Report that Lnk siRNA-transfected endothelial commitment of c-kit (show KIT ELISA Kits)+/Sca-1 (show Ly6a ELISA Kits)+/lineage bone marrow cells have high hematopoietic stem/endothelial progenitor cells (EPCs) colony-forming capacity exhibiting endothelial markers, VE-Cad (show CDH5 ELISA Kits), VEGF (show VEGFA ELISA Kits) and Ang-1 (show ANGPT1 ELISA Kits).
the loss of SH2B3 inhibitory function conferred by the PH domain mutations is mild and may collaborate with JAK2 (show JAK2 ELISA Kits) V617F and CBL (show CBL ELISA Kits) mutations in order to promote either the development or the progression of myeloproliferative neoplasms.
This gene encodes a member of the SH2B adaptor family of proteins, which are involved in a range of signaling activities by growth factor and cytokine receptors. The encoded protein is a key negative regulator of cytokine signaling and plays a critical role in hematopoiesis. Mutations in this gene have been associated with susceptibility to celiac disease type 13 and susceptibility to insulin-dependent diabetes mellitus.
lymphocyte adaptor protein
, SH2B adapter protein 3
, lymphocyte-specific adapter protein Lnk
, signal transduction protein Lnk
, linker of T-cell receptor pathways
, lymphocyte adapter protein