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Our data revealed that HNF1A-AS1 is a direct transactivation target of HNF1alpha in HCC cells and involved in the anti-HCC effect of HNF1alpha. HNF1A-AS1 functions as phosphatase activator through the direct interaction with SHP-1.
this study provided strong in vivo and cellular evidences that hepatocyte SHP-1 plays a cardinal role in the production of inflammatory mediators that contribute to endotoxemia.
actomyosin retrograde flow controls the immune response of primary human Natural killer cells through a novel interaction between beta-actin and the SH2-domain-containing protein tyrosine phosphatase-1 (SHP-1), converting its conformation state, and thereby regulating Natural killer cell cytotoxicity.
Biophysical assay for tethered signaling reactions reveals tether-controlled activity for the phosphatase SHP-1.
This study demonstrates that VB inhibits glioblastoma cell proliferation, migration, and invasion while promoting apoptosis via SHP-1 activation and inhibition of STAT3 phosphorylation.
M. tuberculosis-initiated human mannose receptor signaling regulates macrophage recognition and vesicle trafficking by gamma Fc receptors, Grb2, and SHP-1.
Data suggest that SHP-1/p-STAT3/VEGF-A axis is a potential therapeutic target for metastatic triple-negative breast cancer (TNBC).
these data highlight a signaling pathway in which SHP-1 acts through CrkII to reshape the pattern of Rap1 activation in the immunological synapse.
observations suggest that Chikungunya virus (CHIKV) has the ability to induce host PTPN6 expression, and induction of PTPN6 may favour the attenuation of the pro-inflammatory immune response of the host, which is otherwise detrimental for the survival of CHIKV and establishment of an infection
The results reveal that SHP1 is the long-sought phosphatase that can antagonize Helicobacter pylori CagA. Augmented Helicobacter pylori CagA activity, via SHP1 inhibition, might also contribute to the development of Epstein-Barr virus-positive gastric cancer.
Analyzed gene expression profiles of monocytes from symptomatic congestive heart failure patients; there is a down-regulation of the phosphatase SHP-1 which induces a significant activation of TAK-1/IKK/NF-kB signaling.
crocin induced the expression of SHP-1, a tyrosine protein phosphatase, and pervanadate treatment reversed the crocin-induced downregulation of STAT3, suggesting the involvement of a protein tyrosine phosphatase.
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/Akt-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 and regulated by histone acetylation
The Shp1 functions as a positive regulator and acts in a novel mechanism through promoting EGFR protein expression in human epithelial cells.
Deletion of AT2 receptor reduced SHP-1 activity and restored VEGF actions, leading to an increased blood flow reperfusion after ischemia in diabetes mellitus.
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.
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
Results are consistent with predicted/observed reduction in the Lyn-SHIP-1-PTEN-SHP-1 axis function in B cells from systemic lupus
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(+) and CD8(+) naive T cells in the peripheral lymphoid compartments.
Our study suggests that metformin exerts its insulin sensitizing effects via inhibition of SHP-1 activity and expression.
we found that THEMIS directly regulated the catalytic activity of the tyrosine phosphatase SHP-1.
Studies indicate that SHP1 and SYK crosstalk as a critical regulator of MyD88 post-translational modifications and IL-1-driven inflammation.
Our findings uncover an important role for PP6 as an indispensable guardian of genomic integrity of the lengthy prophase I oocyte arrest, maintenance of primordial follicle pool, and thus female fertility.
The goal of this study was to analyze differentially expressed genes in the bone marrow of mice with NDLD to gain insight into the role of Ptpn6 in myelopoietic bone marrow pathology, and the mechanisms by which Ptpn6 insufficiency in the hematopoietic cells can lead to the development of skin lesions.
the reduction in the positive selection conferred by CD5 overexpression was unaffected by SHP-1 deficiency.
In addition to their role in NK cell activation by hematopoietic cells, the SLAM-SAP-SHP1 pathways influence responsiveness toward nonhematopoietic targets by a process akin to NK cell 'education'.
The prostate of mev/mev mice exhibits signs of aberrant differentiation and the resulting phenotype may be related to the loss of function of SHP-1. Prostatic anomalies in these mice affect, together with defects in sperm maduration, for their sterility.
These studies reveal critical pathways controlled by SHP-1 in oligodendrocytes that relate to susceptibility of SHP-1-deficient mice to both developmental defects in myelination and to inflammatory demyelinating diseases
SHP-1 regulates Cbl-b-mediated T cell responses by controlling its tyrosine phosphorylation and ubiquitination
The inhibitory activity of SHP-1 is needed for setting the threshold of natural killer cell reactivity.
Shp1 signalling is required for the establishment of a life-long protective humoral immunity.
Shp1 binds and controls PIPKIgamma activity and, thereby, modulates phosphatidylinositol (4,5)-bisphosphate levels and adhesion.
CCN1-integrin binding increased the expression of and association between SHP-1 and VEGF-R2, which leads to rapid dephosphorylation of VEGF-R2 tyrosine, thus preventing endothelial cell hyperproliferation.
we present a new hyperinsulinemia animal model and propose ptpn6 as a key mediator triggering hyperinsulinemia-derived insulin resistance and immune suppression.
ptpn6 knockdown induces a spontaneous inflammation-associated phenotype at the late larval stage.
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.
hematopoietic cell phosphatase
, hematopoietic cell protein-tyrosine phosphatase
, protein-tyrosine phosphatase 1C
, protein-tyrosine phosphatase SHP-1
, tyrosine-protein phosphatase non-receptor type 6
, dentatorubro-pallidoluysian atrophy protein
, non-receptor type protein tyrosine phosphatase SHP1
, hemopoietic cell phosphatase
, SH2 phosphatase 1
, protein tyrosine phosphatase, non-receptor type 6 L homeolog