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protooncogene PBF is a negative regulator of p53 function in thyroid tumorigenesis, in which PBF is generally overexpressed and p53 mutations are rare compared with other tumor types
Nnegative pituitary tumor-transforming gene 1 protein-interacting protein (PTTG1IP) immunoexpression predicted a 1.5-fold risk of breast cancer death.
data reveal new insight into PBF function and confirm that, rather than being oncogenic, mutations in PBF are likely to be passenger effects, with overexpression of PBF the more important etiological event in human cancer
PTTG1IP and MAML3 are associated with BHR severity in adult asthma. The relevance of these genes is supported by the eQTL analyses and co-expression of PTTG1lP with vimentin and E-cadherin1, and MAML3 with MAML2.
Findings indicate that PBF and PTTG have a critical role in promoting thyroid cancer that is predictive of poorer patient outcome.
Unique role for PBF in regulating CTTN function to promote endocrine cell invasion and migration.
these results demonstrate an emerging role for PBF in colorectal tumorigenesis through regulating p53 activity, with implications for PBF as a prognostic indicator for invasive tumors.
These findings indicate that miR-584 suppresses glioma cell growth by negatively regulating the expression of PTTG1IP, suggesting that miR-584 has a tumor suppressive role in human glioma pathogenesis.
Data from mutant recombinant proteins suggest that proto-oncogene PBF is a phosphoprotein and highlight importance of tyrosine residue Y174 in both endocytosis of PBF and its interaction/co-localization with NIS/SLC5A5 (sodium-iodide symporter).
PBF expression may be a promising biomarker for prognostic and therapeutic purposes in papillary thyroid carcinoma patients.
Authors identified pituitary tumor-transforming gene 1 (PTTG1) binding factor (PBF) as a target of miR-122 and demonstrated that hepatitis B virus replication causes an obvious increase in PBF levels.
The present study provides the first epidemiological evidence that functional regulatory variants of PTTG1IP were associated with the risk of ER-positive breast cancer, further supporting its relevance as one proto-oncogene in breast cancer.
overexpression of PBF causes thyroid cell proliferation, macrofollicular lesions, and hyperplasia, as well as repression of the critical therapeutic route for radioiodide uptake
PBF's role in endocrine cancer is discussed. [review]
PTTG expression was higher in malignant cells than in primary astrocytes, whereas PTTG-binding factor was not in astrocytoma
overexpression of PTTG and PBF in differentiated thyroid cancer has profound implications for activity of the NIS gene, and hence significantly impacts upon the efficacy of radioiodine treatment.
The encoded protein, which directly binds to pituitary tumor-transforming gene 1 protein (PTTG1), facilitates the nuclear translocation of PTTG1 and potentiates the transcriptional activation of basic fibroblast growth factor by PTTG1. The gene product localizes to both the cytoplasm and nucleus. Its NLS is required for its own nuclear localization, the nuclear localization of PTTG1, and its interaction with PTTG1.
, PTTG-binding factor
, pituitary tumor-transforming gene 1 protein-interacting protein
, pituitary tumor-transforming gene protein-binding factor
, pituitary tumor-transforming 1 interacting protein b