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we report a novel strategy for obtaining ZnZr bimetallic MOFs via the MOF-on-MOF method and exploit them as an aptasensor platform for detecting the cancer marker protein tyrosine kinase-7 (PTK7)
miR2055p is involved in the proliferation, migration and invasion of colorectal cancer cells through inhibiting PTK7.
Higher expression of PTK7 significantly indicates worse prognosis in human malignancies
Inhibition of PTK7 by siRNA treatment significantly decreases the viability of atypical teratoid rhabdoid tumors (ATRT)patient-derived tumor cell lines.These studies provide the groundwork for future preclinical in vivo studies aiming to investigate the efficacy of PTK7 inhibition on ATRT tumor growth
PTK7 localization and protein stability is affected by canonical Wnt ligands.
These findings demonstrate that PTK7 upregulates MMP9 through activation of AP-1 and NF-kappaB and, thus increases invasive properties of ESCC cells.
PTK7 overexpression is associated with esophageal squamous cell carcinoma.
Our data indicate that PTK7 protein expression is associated with the prognosis of oral tongue squamous cell carcinoma
PTK7 expression was correlated with tumor differentiation (P=0.027), lymph node metastasis (P=0.005), distant metastasis (P=0.001) and TNM stage (P=0.028) of colorectal cancer patients
High PTK7 expression is associated with radioresistance in esophageal squamous cell carcinoma.
PTK7 enriches in self-renewing, multipotent stem cells of the human colon.
findings implicate PTK7 as a risk factor for NTDs and provide additional evidence for a pathogenic role of PCP signaling in these malformations
overexpression in PTK7-negative cancer cells led to increased metastatic events. PTK7 expression thus represents a potential prognostic biomarker and a novel therapeutic target in CRC.
data demonstrates that PTK7 regulates the activity of KDR biphasically by inducing oligomerization of KDR molecules at lower concentrations and by surrounding KDR molecules at higher concentrations.
PTK7 regulates Id1 expression in CD44-high glioma cell lines. Targeting PTK7 could be an effective strategy for treating glioma with high CD44 expression.
The results suggest that N-acylethanolamine acid amidase and protein tyrosine kinase 7 may be used as potential tissue biomarkers to avoid overtreatment of non-aggressive prostate cancer
Expression level of PTK7 was significantly decreased from benign to malignant ovarian epithelial tumors. survival analysis showed that patients with negative expression of PTK7 protein had poorer outcome than those with positive expression.
PTK7 acts as a cancer-related gene and may be a potent prognostic marker for Hepatocellular carcinoma(HCC).
results provide convincing evidence that both PTK7 expression and proteolysis, rather than the level of the cellular full-length PTK7 alone, contribute to efficient directional cell motility and metastasis in cancer
Furthermore, we confirmed that these phenotypic changes are associated with the inactivation of AKT and ERK. Our findings suggest that PTK7 has different oncogenic roles in organs and target tumors.
PTK7 regulates extracellular matrix integrity and the activity levels of RAC1 and myosin II, which in turn regulates Wolffian duct morphogenesis and therefore, epididymal function.
In a Ptk7-deficient mouse strain, loss of Ptk7 leads to a diminished pool of hematopoietic stem cells but does not affect in vitro or in vivo differentiation. This is correlated with increased quiescence and reduced homing abilities of Ptk7-deficient hematopoietic stem and progenitor cells.
Data suggest that protein tyrosine kinase 7 (PTK7) is essential for Wolffian duct morphogenesis and male fertility.
PTK7 expression plays an important role in the invasiveness of intrahepatic cholangiocarcinoma cells.
Planar polarity of neural cell motility and intercalation requires Ptk7 function.
acts in conjunction with the noncanonical Wnt pathway to orient epithelial planar cell polarity through modulation of myosin II-based contractile tension between supporting cells and hair cells
The tyrosine kinase receptor, PTK7, is implicated in beta-catenin-dependent developmental processes.
These findings illustrate a novel and pivotal role for Cdx function upstream of Ptk7 and neural tube closure in vertebrates.
Chuzhoi mutation, that causes multiple abnormalities maps, to Chromosome 17 and carries a splice site mutation in Ptk7 and causes disruption of Ptk7 protein expression.
Ptk7 mRNA was expressed at high levels in lung and un-pregnant uterus among adult tissues, and in the tail, limbs, somites, gut, and craniofacial regions among embryonic tissues, and suggest that PTK7 plays multiple roles in embryonic development.
a mutation disrupts neural tube closure and stereociliary bundle orientation, and shows genetic interactions with a mutation in the mouse Van Gogh homologue vangl2
polarized cell behaviors underlying CE in the mouse, clearly define specific roles for planar polarity and for the novel planar cell polarity gene, Ptk7, as essential regulators of mediolateral cell intercalation during mammalian CE.
This gene encodes a member of the receptor protein tyrosine kinase family of proteins that transduce extracellular signals across the cell membrane. The encoded protein lacks detectable catalytic tyrosine kinase activity, is involved in the Wnt signaling pathway and plays a role in multiple cellular processes including polarity and adhesion. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
PTK7 protein tyrosine kinase 7
, inactive tyrosine-protein kinase 7
, tyrosine-protein kinase-like 7-like
, colon carcinoma kinase 4
, pseudo tyrosine kinase receptor 7
, tyrosine-protein kinase-like 7
, serum response factor
, protein chuzhoi
, protein-tyrosine kinase 7
, receptor tyrosine kinase-like protein
, kinase-like protein