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p53, also known as Tumor protein P53, cellular tumor antigen p53 (UniProt name), or transformation-related protein 53 (TRP53) is a regulatory protein that is often mutated in human cancers. The p53 proteins (originally thought to be, and often spoken of as, a single protein) are crucial in vertebrates, where they prevent cancer formation. [5]
Neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's are all age-related diseases and involve increased apoptosis where cells die that are still able to function or that contribute to support function of tissue. Apaf-1-ALT is an Apaf-1 mutant found in prostate cancer, which does not have residues 339-1248.
Li–Fraumeni syndrome is characterized by early onset of cancer, a wide variety of types of cancers, and development of multiple cancers throughout one's life. [8] LFS: Mutations in TP53. TP53 is a tumor suppressor gene on chromosome 17 that normally assists in the control of cell division and growth through action on the normal cell cycle.
Protein phosphorylation is a reversible post-translational modification of proteins in which an amino acid residue is phosphorylated by a protein kinase by the addition of a covalently bound phosphate group. Phosphorylation alters the structural conformation of a protein, causing it to become activated, deactivated, or otherwise modifying its ...
A suicide gene is a gene which will cause a cell to kill itself through apoptosis. Suicide gene therapy involves delivery of a gene which codes for a cytotoxic product into tumor cells. [6] This can be achieved by two approaches, indirect gene therapy and direct gene therapy. Indirect gene therapy employs enzyme-activated prodrug, in which the ...
The p53 upregulated modulator of apoptosis (PUMA) also known as Bcl-2-binding component 3 (BBC3), is a pro- apoptotic protein, member of the Bcl-2 protein family. [5][6] In humans, the Bcl-2-binding component 3 protein is encoded by the BBC3 gene. [5][6] The expression of PUMA is regulated by the tumor suppressor p53.
Cancer is caused by genetic changes leading to uncontrolled cell growth and tumor formation. The basic cause of sporadic (non-familial) cancers is DNA damage and genomic instability. [1][2] A minority of cancers are due to inherited genetic mutations. [3] Most cancers are related to environmental, lifestyle, or behavioral exposures. [4]
Familial adenomatous polyposis (FAP) is an autosomal dominant inherited condition in which numerous adenomatous polyps form mainly in the epithelium of the large intestine. While these polyps start out benign, malignant transformation into colon cancer occurs when they are left untreated. Three variants are known to exist, FAP and attenuated ...