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The expression of PTP1B in skeletal muscle was increased after caloric restriction and prolonged exercise.
preliminary data show that heterozygous or homozygous deletion of PTPN1 increases the severity of MPN (zeige PRSS27 Proteine) in Jak2V617F-knock-in mice. Future studies will determine whether loss of PTPN1 cooperates with the JAK2V617F mutation in the pathogenesis of MPN (zeige PRSS27 Proteine)
we demonstrated a novel oncogenic mechanism of PTP1B on affecting PITX1 (zeige PITX1 Proteine)/p120RasGAP (zeige RASA1 Proteine) in colorectal carcinoma(CRC (zeige CALR Proteine)). Regorafenib inhibited CRC (zeige CALR Proteine) survival through reserving PTP1B-dependant PITX1 (zeige PITX1 Proteine)/p120RasGAP (zeige RASA1 Proteine) downregulation. PTP1B may be a potential biomarker predicting regorafenib effectiveness, and a potential solution for CRC (zeige CALR Proteine)
this study highlights an important role for Nck1 (zeige NCK1 Proteine) in fine-tuning IRE1alpha (zeige ERN1 Proteine) expression and signaling that regulate PTP1B expression and subsequent activation of the PI3K (zeige PIK3CA Proteine)-Akt (zeige AKT1 Proteine) pathway in HepG2 cells.
In conclusion, HDAC6 (zeige HDAC6 Proteine) might enhance aggressive melanoma cells progression via interacting with PTPN1, which was independent of its histone modifying activity.
PTP1B is widely expressed in the human breast gland with highest expression in myoepithelial cells and fibroblasts. Inhibition of PTP1B in D492 and HMLE affects cell-cell adhesion and induces anoikis-like effects.
The results of the present study highlight the expression quantitative trait loci enrichment and pleiotropy in psoriasis and schizophrenia, and also suggest a possible key role of the PTPN1 gene in the etiology of psoriasis
The structural fragments which are important for PTP1B inhibition were identified by naive Bayesian method and can be further exploited to design new molecules around the identified scaffolds. The descriptive and predictive modeling strategy applied in this study is capable of identifying PTP1B inhibitors from the large compound libraries
The gained results are observed not only the unbinding mechanism of IRK (zeige KCNJ12 Proteine)-PTP1B complexes came from pulling force profile, number of hydrogen bonds, and interaction energy between IRK (zeige KCNJ12 Proteine) and PTP1Bs but also described PTP1B's point mutations could variably change its binding affinity towards IRK (zeige KCNJ12 Proteine).
these results suggest that inhibition of PTP1B activity is a promising new target in the treatment of colorectal cancer and the prevention of metastasis
PTP1B gene deletion significantly limited CLP (zeige HAPLN1 Proteine)-induced insulin (zeige INS Proteine) resistance, improved AMP-activated protein kinase (zeige PRKAA2 Proteine) signaling pathway and Glucose Transporter 4 translocation, and decreased inflammation. These effects were associated with a reduction of sepsis-induced endothelial dysfunction/impaired NO production and especially of insulin (zeige INS Proteine)-mediated dilatation.
Sleep fragmentation induces increased food intake, reduced leptin (zeige LEP Proteine) signaling in hypothalamus, systemic insulin (zeige INS Proteine) resistance, and reduced visceral white adipose tissue insulin (zeige INS Proteine) sensitivity and inflammation that are mediated by increased PTP-1B activity.
S-nitrosylation of endogenous SHP2 (zeige PTPN11 Proteine) Phosphatase and PTP1B in endothelial insulin (zeige INS Proteine) signaling has been demonstrated.
The findings show that reduced PTP1B responses contribute to disease symptoms in part by enhancing S100A9 (zeige S100A9 Proteine) expression during viral-associated chronic obstructive pulmonary disease exacerbations.
Under normoglycemia control and pod-PTP1B KO mice exhibited comparable renal functions. However, podocyte PTP1B disruption attenuated hyperglycemia-induced albuminuria and renal injury and preserved glucose control. Also, podocyte PTP1B disruption was accompanied with improved renal insulin (zeige INS Proteine) signaling and enhanced autophagy with decreased inflammation and fibrosis.
Endothelial PTP1B deletion improves cardiac VEGF (zeige VEGFA Proteine) signalling and angiogenesis and protects against chronic afterload-induced heart failure.
PTP1B inhibitors protect against atherosclerotic plaque formation in the LDLR (zeige LDLR Proteine)(-/-) mouse model of atherosclerosis.
The results suggest a deficiency of PTP1B improves hypothalamic insulin (zeige INS Proteine) sensitivity resulting in the attenuation of AgRP (zeige AGRP Proteine) mRNA expression under HFD conditions.
cadherin 2 (CDH2 (zeige CDH2 Proteine)) and CDH4 (zeige CDH4 Proteine) cooperate to regulate radial migration in mouse brain via the protein tyrosine phosphatase 1B (PTP1B) and alpha- and beta-catenins.
this paper shows that PTP1B specifically regulates IgE-mediated STAT5 (zeige STAT5A Proteine) pathway, but is redundant in influencing mast cell function in vivo
PTP-1B increased posthypoxia by about 30% and persisted for 2 weeks while Src kinase (zeige CSK Proteine) inhibition attenuated the expected PTP-1B-increased expression.
data for the first time demonstrate a calpain/PTP1B/VEGFR2 negative feedback loop in the regulation of VEGF-induced angiogenesis. Modulation of local PTP1B and/or calpain activities may prove beneficial in the treatment of impaired wound healing in diabetes.
The protein encoded by this gene is the founding member of the protein tyrosine phosphatase (PTP) family, which was isolated and identified based on its enzymatic activity and amino acid sequence. PTPs catalyze the hydrolysis of the phosphate monoesters specifically on tyrosine residues. 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. This PTP has been shown to act as a negative regulator of insulin signaling by dephosphorylating the phosphotryosine residues of insulin receptor kinase. This PTP was also reported to dephosphorylate epidermal growth factor receptor kinase, as well as JAK2 and TYK2 kinases, which implicated the role of this PTP in cell growth control, and cell response to interferon stimulation.
protein tyrosine phosphatase, non-receptor type 1
, tyrosine-protein phosphatase non-receptor type 1
, tyrosine-protein phosphatase non-receptor type 1-like
, protein tyrosine phosphatase, placental
, protein-tyrosine phosphatase 1B
, protein-protein-tyrosine phosphatase HA2
, protein-tyrosine phosphatase HA2
, protein tyrosine phosphatase 1b
, non-receptor protein tyrosine phosphatase
, phosphoprotein phosphatase
, tyrosine phosphatase 1B