نتایج جستجو برای: her 2 proto oncogene protein
تعداد نتایج: 3535071 فیلتر نتایج به سال:
The RET proto-oncogene has been identified as the multiple endocrine neoplasia type 2 disease gene. An association between specific RET mutation and disease phenotype has been reported. We present the phenotype-genotype of 12 Greek families with multiple endocrine neoplasia type 2A (MEN 2A) or familial medullary thyroid carcinoma (FMTC). Seventy members were studied and DNA analysis for RET mut...
Alzheimer's disease (AD) is a degenerative brain with complex clinical manifestations and pathogeneses such as abnormal deposition of beta-amyloid protein inflammation caused by the excessive activation microglia. CXC motif chemokine receptor type 4 (CXCR4) G protein-coupled that binds to ligand 12 (CXCL12) activate downstream signaling pathways, Janus kinase/signal transducer activator transcr...
Recognition of tumor cells by cytolytic T lymphocytes depends on cell surface MHC class I expression. As a mechanism to evade T cell recognition, many malignant cancer cells, including those of prostate cancer, downregulate MHC class I. For the majority of human cancers, the molecular mechanism of MHC class I down regulation is unclear, although it is well established that MHC class I down-regu...
SnoN was first identified based on its homology with the proto-oncogene c-Ski, and has since been implicated as a promoter of oncogenic transformation and cancer progression. Consistent with a role as proto-oncogene, SnoN negatively regulates TGF-beta signalling, through its interactions with Smad complexes. Thus, SnoN inhibits the growth inhibitory effect of TGF-beta, which is considered as th...
-Catenin controls both cadherin-mediated cell adhesion and activation of Wnt target genes. We demonstrate here that the -catenin-binding protein BCL9-2, a homolog of the human proto-oncogene product BCL9, induces epithelial–mesenchymal transitions of nontransformed cells and increases -catenin-dependent transcription. RNA interference of BCL9-2 in carcinoma cells induces an epithelial phenotype...
I NSIGHT into normal and abnormal cell growth and differentiation may be obtained by identifying and analyzing the activity of highly specific genes, called oncogenes, whose coding sequences contain the information necessary to initiate and maintain neoplastic transformation. The identification of oncogenes and the characterization of the structure and function of these genes have progressed ra...
The products of proto-oncogene play critical roles in the development or maintenance of multicellular societies in animals via strict regulatory systems. When these regulatory systems are disrupted, proto-oncogenes can become oncogenes, and thereby induce cell transformation and carcinogenesis. To understand the molecular basis for development of the regulatory system of proto-oncogenes during ...
In a total of 83 UN specimens were investigated for proto-oncogene mutations, tumor supressor genes promoter methylation status and c-myc and Ki-67 expression. Point mutations in c-myc were detected in cases with high grade and proliferation index. Mutated K-ras proto-oncogene profiles were detected in 17 (21%) tumoral spiecemens that examined. Tumor specimens were also showed hypermethylated p...
The study of oncogenic viruses led to the discovery that transforming retroviruses contain oncogenes homologous with and/or derived from cellular proto-oncogenes. In humans malignant transformation is often the result of the activation of proto-oncogenes. Normal proto-oncogenes can be activated to transforming proto-oncogenes by a variety of mechanisms including point mutation, translocation an...
Spitz nevus (SN) is predominantly distributed throughout the lower extremities, while an acral location rare. Since SN occasionally resembles clinicopathological presentation of malignant melanoma (MM), it presents a diagnostic challenge, especially on glabrous skin. Past reports suggest that several genetic aberrations are associated with specific subtypes melanocytic tumors. Immunohistochemis...
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