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Low PTPN2 protein expression was found in 50.2% of the breast tumours (110/219), gene copy loss in 15.4% (33/214). Low protein expression was associated with a higher relapse rate in patients with Luminal A and HER2-positive tumours, but not triple-negative tumours.
A dual role for myeloid PTPN2 in directly regulating inflammasome activation and IL-1beta production to suppress pro-inflammatory responses during colitis but promote intestinal tumor development, is reported.
Further comparison of alanine scanning demonstrates that the reduction in the energy contribution of Arg254 caused by A27S mutation leads to a different inhibitory activity. These observations provide novel insights into the selective binding mechanism of PTP1B inhibitors to TCPTP
The higher levels of PTPN2 were associated with a worse overall survival both in patients with gliomas and glioblastomas.
This study shows that a PTPN2-rs7234029 polymorphism is associated with ocular Behcet's disease and is strongly influenced by gender. In addition, our results suggest that the genetic association with PTPN2 may involve the regulation of PTPN2 mRNA expression and cytokine secretion.
PTPN2 negatively regulates Akt signalling and loss of PTPN2 protein along with increased pAkt-n is a new potential clinical marker of endocrine treatment efficacy in breast cancer
RA samples with PTPN2:rs478582 and/or PTPN22:rs2476601 were more positive for MAP than samples without polymorphisms. Combined occurrence of PTPN2:rs478582 and PTPN22:rs2476601 in association with the presence of MAP has significantly increased T-cell response and elevated IFN-gamma expression in RA samples.
our data indicate a novel role for PTPN2 and PTPN22 in controlling intestinal microbiota composition and further elucidate the complex interplay between genetic risk factors, intestinal microbiota and disease course in IBD patients.
The results provide the first indication that PTPN2 variants contribute to the risk of Type 1A diabetes, and possibly induce non-specific Type 1A diabetes.
PTPN2, an anti-inflammatory factor regulated by VDR, was reduced in type 2 diabetics with chronic kidney disease stages 1-2.
PTPN2 genetic polymorphisms are associated with psoriasis in the Northeastern Chinese population.
PTPN2 rs2847297 and rs2847282 may be potential susceptible loci for lung cancer risk.
Data suggests that SNPs in PTPN2/22 affect the negative regulation of the immune response in Crohn's disease patients, thus leading to an increase in inflammation/apoptosis and susceptibility of mycobacteria.
the molecular mechanisms by which PTP1B and TC-PTP loss co-operates with other genetic aberrations will need to be elucidated to design more effective therapeutic strategies.
In summary, we demonstrate that TCPTP protects the intestinal epithelial barrier by restricting STAT-induced claudin-2 expression.
PASD1 serves as a critical nuclear positive regulator of STAT3-mediated gene expression and tumorigenesis.
PTPN2_rs1893217 CC was associated with a lower risk of having joints with Limitation of motion in patients with Juvenile Idiopathic Arthritis.
reported that SNPs in STAT4, PTPN2, PSORS1C1, and TRAF3IP2 are associated with response to TNF-i treatment in RA patients; however, these findings should be validated in a larger population
The results suggest that miR-448 might promote Th17 differentiation in multiple sclerosis and thus aggravate the disease through inhibiting PTPN2.
ACPA were associated significantly with rs7574865 in STAT-4. The SNP rs2233945 in the PSORS1C1 gene was protective regarding the presence of bone erosions, while rs2542151 in PTPN2 gene was associated with joint damage.
PTPN2 is an essential STAT3 repressor involved in the maintenance and induction of naive pluripotency.
Our findings reveal that TC-PTP has potential as a novel target for the prevention of skin cancer through its role in the regulation of STAT3 and AKT signaling.
TCPTP controls Insulin resistance signaling in AgRP neurons to coordinate hepatic glucose production and brown/beige adipocyte glucose uptake in response to feeding/fasting.
PTPN2 overexpression in white adipose tissue could significantly reduce macrophages infiltration, the ratio of M1/M2 macrophages and the expression of pro-inflammatory cytokines in white adipose tissue , improving insulin resistance.
Data suggest that interaction of Ppard with Tcptp45 blunts insulin resistance and leads to retention of Tcptp45 in nucleus of hepatocytes, myotubes, and adipocytes; alteration of such interactions may be involved in insulin resistance observed in obesity. (Ppard = peroxisome proliferator activator receptor delta; Tcptp45 = protein tyrosine phosphatase non-receptor type 2 [Ptpn2], 45kDa alternative splicing variant)
These results indicate that deficiencies in PTPN2 across multiple immune lineages, including naive T cells, Tfh cells and B cells, contribute to the development of autoimmunity.
regulates T cell lineage commitment and alphabeta versus gammadelta specification
PTPN2 is a positive regulator of lipopolysaccharide-induced inflammatory response by enhancing the activity of Src through targeting the inhibitory phosphor-tyrosine527 of Src.
Loss of PTPN2 in intestinal epithelial cells has no significant influence on inflammation in dextran sulphate sodium-induced colitis. On the other hand, loss of PTPN2 induced enhanced epithelial cell proliferation and promoted wound closure.
Antigen receptor-mediated depletion of FOXP3 in induced regulatory T-lymphocytes via PTPN2 and FOXO1
A novel role for TCPTP in insulin secretion and uncover STAT3 as a physiologically relevant target for TCPTP in the endocrine pancreas.
dysfunction of PTPN2 results in aberrant T-cell differentiation and intestinal dysbiosis similar to those observed in human CD. Our findings indicate a novel and crucial role for PTPN2 in chronic intestinal inflammation.
PTPN2 attenuates T-cell lymphopenia-induced proliferation.
demonstrate that SIPAR directly interacts with T cell protein tyrosine phosphatase TC45 and enhances its association with STAT3
findings reveal a mechanism by which PTPN2 SNPs might convert a tolerogenic CD8(+) T cell response into one capable of causing the destruction of pancreatic beta-cells.
TC-PTP inhibits STAT3-mediated mouse keratinocyte skin cell proliferation and survival following UVB irradiation.
Data suggest that spermidine supplementation and subsequent protein tyrosine phosphatase non-receptor type 2 (PTPN2) activation may be helpful in the treatment of chronic intestinal inflammation.
cleavage of TCPTP by NS3/4A induces a shift of the intrahepatic immune response toward a nonantiviral Th2-dominated immunity. These effects are reversed by ribavirin.
Homozygous TC-PTP deficiency in murine mammary fat pads in vivo is associated with elevated Src family PTKs and STAT3 signaling.
The protein encoded by this gene is a member of the protein tyrosine phosphatase (PTP) family. Members of the PTP family share a highly conserved catalytic motif, which is essential for the catalytic activity. PTPs are known to be signaling molecules that regulate a variety of cellular processes including cell growth, differentiation, mitotic cycle, and oncogenic transformation. Epidermal growth factor receptor and the adaptor protein Shc were reported to be substrates of this PTP, which suggested the roles in growth factor mediated cell signaling. Multiple alternatively spliced transcript variants encoding different isoforms have been found. Two highly related but distinctly processed pseudogenes that localize to chromosomes 1 and 13, respectively, have been reported.
T-cell protein tyrosine phosphatase
, tyrosine-protein phosphatase non-receptor type 2
, T cell protein-tyrosine phosphatase
, protein-tyrosine phosphatase PTP-2
, protein-tyrosine phosphatase PTP-S
, phosphoprotein phosphatase
, protein tyrosine phosphatase 1B
, protein tyrosine phosphatase, non-receptor type 2, like
, protein tyrosine phosphatase, non-receptor type 2, a
, protein tyrosine phosphatase, non-receptor type 2 L homeolog