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Deletion of AT2 receptor reduced SHP-1 activity and restored VEGF actions, leading to an increased blood flow reperfusion after ischemia in diabetes mellitus.
SHP (show LAMC1 ELISA Kits) deficiency protects myocardia from lipid accumulation in high fat diet-fed mice.
These findings show a novel role for Shp-1 in the regulation of IEC growth and secretory lineage allocation, possibly via modulation of PI3K/Akt (show AKT1 ELISA Kits)-dependent signaling pathways.
These findings suggest that protein tyrosine phosphatase SHP-1 may act as a positive regulator of osteoblast differentiation through direct association with and dephosphorylation of GSK3beta (show GSK3b ELISA Kits).
data establish SHP-1 as a critical player in setting the threshold downstream of TCR signaling and identify a novel function of SHP-1 as a regulator of T cell susceptibility to Treg-mediated suppression in vitro and in vivo
human microbiota was able to reduce the levels of tauro-beta-muricholic acid and induce expression of FXR (show NR1H4 ELISA Kits) target genes Fgf15 and Shp (show LAMC1 ELISA Kits) in ileum after long-term colonization. We show that a human microbiota can change BA composition and induce FXR (show NR1H4 ELISA Kits) signaling in colonized mice, but the levels of secondary BAs produced are lower than in mice colonized with a mouse microbiota
SHP (show LAMC1 ELISA Kits) and REV-ERBalpha (show NR1D1 ELISA Kits) play a critical role in controlling rhythmic CHOP (show DDIT3 ELISA Kits) expression in alcoholic fatty liver
Results are consistent with predicted/observed reduction in the Lyn-SHIP-1-PTEN-SHP-1 axis function in B cells from systemic lupus
our results suggest that SHP (show LAMC1 ELISA Kits) upregulation upon high-fat feeding leads to lipid accumulation, insulin (show INS ELISA Kits) resistance and inflammation in cardiomyocytes.
Our data show that SHP1 is required for the survival of mature thymocytes and the generation of the functional T-cell repertoire, as its absence leads to a reduction in the numbers of CD4 (show CD4 ELISA Kits)(+) and CD8 (show CD8A ELISA Kits)(+) naive T cells in the peripheral lymphoid compartments.
crocin induced the expression of SHP-1, a tyrosine protein phosphatase, and pervanadate treatment reversed the crocin-induced downregulation of STAT3 (show STAT3 ELISA Kits), suggesting the involvement of a protein tyrosine phosphatase (show ACP1 ELISA Kits).
this review focalizes upon the implication of SHP-1 in the pathogenesis of autoimmune disorders, and addresses developing therapeutic strategies targeting SHP-1
we demonstrated that SHP-1 dephosphorylates PKM2Y105 to inhibit the Warburg effect and nucleus-dependent cell proliferation, and the dephosphorylation of PKM2Y105 by SHP-1 determines the efficacy of targeted drugs for hepatocellular carcinoma treatment
These findings have provided first lines of evidences that PDZK1 expression is negatively correlated with SHP-1 activation and poor clinical outcomes in clear cell renal cell carcinoma (ccRCC) . PDZK1 was identified as a novel tumor suppressor in ccRCC by negating SHP-1 activity
luteolin inhibited STAT3 activation through disrupting the binding of HSP-90 to STAT3, which promoted its interaction to SHP-1.
These findings show a novel role for Shp-1 in the regulation of IEC growth and secretory lineage allocation, possibly via modulation of PI3K (show PIK3CA ELISA Kits)/Akt (show AKT1 ELISA Kits)-dependent signaling pathways.
the role of Shp1 in myeloid cells and how its dysregulation affects immune function, which can impact human disease.
PTPN6 is associated with progression of chronic myeloid leukaemia. Low expression level of PTPN6 was associated with DNA methylation (show HELLS ELISA Kits) and regulated by histone acetylation
The Shp1 functions as a positive regulator and acts in a novel mechanism through promoting EGFR (show EGFR ELISA Kits) protein expression in human epithelial cells.
SHP1 DNA methylation (show HELLS ELISA Kits) in in patients with B cell non-Hodgkin lymphoma
The protein encoded by this gene is a member of the protein tyrosine phosphatase (PTP) family. PTPs are known to be signaling molecules that regulate a variety of cellular processes including cell growth, differentiation, mitotic cycle, and oncogenic transformation. N-terminal part of this PTP contains two tandem Src homolog (SH2) domains, which act as protein phospho-tyrosine binding domains, and mediate the interaction of this PTP with its substrates. This PTP is expressed primarily in hematopoietic cells, and functions as an important regulator of multiple signaling pathways in hematopoietic cells. This PTP has been shown to interact with, and dephosphorylate a wide spectrum of phospho-proteins involved in hematopoietic cell signaling. Multiple alternatively spliced variants of this gene, which encode distinct isoforms, have been reported.
nuclear receptor subfamily 0 group B member 2
, orphan nuclear receptor SHP
, small heterodimer partner
, hematopoietic cell phosphatase
, hematopoietic cell protein-tyrosine phosphatase
, protein-tyrosine phosphatase 1C
, protein-tyrosine phosphatase SHP-1
, tyrosine-protein phosphatase non-receptor type 6
, hemopoietic cell phosphatase
, SH2 phosphatase 1
, dentatorubro-pallidoluysian atrophy protein
, non-receptor type protein tyrosine phosphatase SHP1