نتایج جستجو برای: tumor suppressor protein p53
تعداد نتایج: 1594311 فیلتر نتایج به سال:
p53, a tumor suppressor and a transcription factor, binds DNA in a sequence-specific manner. In more than half of human cancers, p53 has been found to be mutated with the loss of DNA-binding ability. In this review, we focus on the sensitive detection of interaction of tumor suppressor p53 with double-stranded DNA bearing the consensus sequence and proteins, such as monoclonal antibodies recogn...
p53 is a powerful tumor suppressor and is an attractive cancer therapeutic target because it can be functionally activated to eradicate tumors. The gene encoding p53 protein is mutated or deleted in half of human cancers, which inactivates its tumor suppressor activity. In the remaining cancers with wild-type p53 status, its function is effectively inhibited through direct interaction with the ...
The dynamic alterations in the cytoskeletal components actin and intermediate, etc. filaments are required for cell invasion migration. cytoskeleton is a highly structure that governed by delicate balance of filament formation disassembly. To controlling activities key epithelial mesenchymal transition (EMT) could be viable solution to metastasis. Bioinformatics technologies also allow research...
The p53 tumor suppressor exerts a variety of cell-autonomous effects that are aimed to thwart tumor development. In addition, however, there is growing evidence for cell nonautonomous tumor suppressor effects of p53. In the present study, we investigated the impact of stromal p53 on tumor growth. Specifically, we found that ablation of p53 in fibroblasts enabled them to promote more efficiently...
Tribbles 1 (TRB1) is one of the mammalian orthologs of Drosophila Tribbles, which regulates development and cell proliferation. TRB1 is suggested to act as a scaffold protein in signaling pathways for important cellular processes. TRB1 has also been identified as a myeloid oncogenic driver and mediates leukemogenesis through the mitogen-activated protein extracellular kinase (MEK)/extracellular...
background:non-melanoma skin cancer (nmsc), the most prevalent types being squamous cell carcinoma (scc) and basal cell carcinoma (bcc), is the most common type of malignancy in human beings. these neoplasms are more frequent in the elderly and fair skinned people and mainly occur on sun-exposed sites of the body. ultraviolet b (uvb) has a well-known effect in induction and promotion of growth ...
The PTEN tumor suppressor protein inhibits phosphatidylinositol 3-kinase (PI3K)/Akt signaling that promotes translocation of Mdm2 into the nucleus. When restricted to the cytoplasm, Mdm2 is degraded. The ability of PTEN to inhibit the nuclear entry of Mdm2 increases the cellular content and transactivation of the p53 tumor suppressor protein. Retroviral transduction of PTEN into U87MG (PTEN nul...
objective(s) p53 is an important tumor suppressor, which is mutated in later stages of many cancers and leads to resistance to chemotherapy. the aim of this study was to reveal mutations of tp53 in colorectal cancer in kerman province. materials and methods a total of forty-three colon cancer specimens as paraffin block or fresh tissues, which passed stage iiia, were selected. three exons 5, 7 ...
Tumor suppressor protein promyelocytic leukemia (PML) is implicated in apoptosis regulation and antiviral response. PML localizes predominantly to PML-nuclear bodies (PML-NB), nuclear macromolecular complexes regulating tumor suppressor protein p53 activity. Consistent with the function of PML in the cellular antiviral response, PML-NBs represent preferential targets in viral infections. In the...
the p53 protein is expressed in all normal cells and appears to function in cell cycle regulation. abnormally higli levels of the protein are found in many different types of cancer. in breast cancer, overexpression of p53 is associated with point mutations within highly conserved regions of the p53 gene. these altered genes encode stable p53 protein that can be detected by standard immunohisto...
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