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thyroid neoplasms/proliini
Linkki tallennetaan leikepöydälle
12 tuloksia
Proline homozygosity in codon 72 of p53 is a factor of susceptibility for thyroid cancer.
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A common germline polymorphism of p53 gene produces an Arginine to Proline change at aminoacid position 72. The resulting codon 72 variants have been reported associated with tumor susceptibility since they reduce p53 ability to activate apoptosis. Codon 72 polymorphism may play a role in subside
Overexpression of cellular activity and protein level of protein kinase FA/GSK-3 alpha correlates with human thyroid tumor cell dedifferentiation.
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Computer analysis of protein phosphorylation sites sequence revealed that transcriptional factors and viral oncoproteins are prime targets for regulation of proline-directed protein phosphorylation, suggesting an association of the proline-directed protein kinase (PDPK) family with neoplastic
Three-dimensional telomere dynamics in follicular thyroid cancer.
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BACKGROUND
Over the last decade, annual incidence rates for thyroid cancer have been among the highest of all cancers in the Western world. However, the genomic mechanisms impacting thyroid carcinogenesis remain elusive.
METHODS
We employed an established mouse model of follicular thyroid cancer
Significant association of TP53 Arg72Pro polymorphism in susceptibility to differentiated thyroid cancer.
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BACKGROUND
Among various polymorphic variants of TP53 gene, codon 72 polymorphism (Arg72Pro) has been found to be associated with cancer susceptibility, but only few studies have investigated their effect on thyroid cancer risk.
OBJECTIVE
A case control study was conducted to elucidate the possible
Misregulation of the proline rich homeodomain (PRH/HHEX) protein in cancer cells and its consequences for tumour growth and invasion.
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The proline rich homeodomain protein (PRH), also known as haematopoietically expressed homeobox (HHEX), is an essential transcription factor in embryonic development and in the adult. The PRH protein forms oligomeric complexes that bind to tandemly repeated PRH recognition sequences within or at a
BAG3 sensitizes cancer cells exposed to DNA damaging agents via direct interaction with GRP78.
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Bcl-2 associated athanogene 3 (BAG3) has a modular structure that contains a BAG domain, a WW domain, a proline-rich (PxxP) domain to mediate potential interactions with chaperons and other proteins that participate in more than one signal transduction. In search for novel interacting partners, the
Polymorphisms within base and nucleotide excision repair pathways and risk of differentiated thyroid carcinoma.
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The thyrocytes are exposed to high levels of oxidative stress which could induce DNA damages. Base excision repair (BER) is one of the principal mechanisms of defense against oxidative DNA damage, however recent evidences suggest that also nucleotide excision repair (NER) could be involved. The aim
Evidences that the polymorphism Pro-282-Ala within the tumor suppressor gene WWOX is a new risk factor for differentiated thyroid carcinoma.
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We report a hypothesis-driven study aimed to detect genetic markers of susceptibility to differentiated thyroid carcinomas (DTC). A large number of candidate genes were first selected through literature search (genome-wide studies were also included). To restrict the analysis to single nucleotide
Mdm4 loss in mice expressing a p53 hypomorph alters tumor spectrum without improving survival.
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The p53 pathway is inactivated in most human cancers, and its reactivation in tumors appears as a promising therapeutic strategy. Overexpression of Mdm4, a p53 negative regulator, occurs in a significant fraction of human cancers. Mouse models were used to evaluate the therapeutic potential of
Roles of XB130, a novel adaptor protein, in cancer.
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Adaptor proteins, with multi-modular structures, can participate in the regulation of various cellular functions. During molecular cloning process of actin filament associated protein, we have discovered a novel adaptor protein, referred to as XB130. The human xb130 gene is localized on chromosome
PRH/HHex inhibits the migration of breast and prostate epithelial cells through direct transcriptional regulation of Endoglin.
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PRH/HHex (proline-rich homeodomain protein) is a transcription factor that controls cell proliferation and cell differentiation in a variety of tissues. Aberrant subcellular localisation of PRH is associated with breast cancer and thyroid cancer. Further, in blast crisis chronic myeloid leukaemia,
Amino acid response by Halofuginone in Cancer cells triggers autophagy through proteasome degradation of mTOR.
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