TPP1
Tumor Protein P53 Inducible Nuclear Protein 2 | |||||||
---|---|---|---|---|---|---|---|
Identifiers | |||||||
Symbol | ? | ||||||
HGNC | 20345 | ||||||
OMIM | 608201 | ||||||
RefSeq | NM_018438 | ||||||
UniProt | Q8IXH9 | ||||||
|
Tumor Protein P53 Inducible Nuclear Protein 2 (TP53INP2), also known as DOR (Diabetes- and Obesity-regulated gene), is a protein that in humans is encoded by the TP53INP2 gene. This protein is involved in several cellular processes, including autophagy, cell cycle regulation, and apoptosis.
Structure[edit | edit source]
TP53INP2 is a nuclear protein that contains several functional domains, including a nuclear localization signal (NLS) and a domain that interacts with autophagy-related proteins. The protein is approximately 220 amino acids in length and has a molecular weight of about 25 kDa.
Function[edit | edit source]
TP53INP2 plays a critical role in the regulation of autophagy, a cellular process that degrades and recycles cellular components. It acts as a co-activator of autophagy by interacting with autophagy-related proteins such as LC3 and GABARAP. TP53INP2 is also involved in the regulation of the cell cycle and apoptosis, particularly in response to stress signals such as DNA damage.
Role in Autophagy[edit | edit source]
TP53INP2 enhances the formation of autophagosomes by facilitating the recruitment of LC3 to the autophagosome membrane. This process is crucial for the degradation of damaged organelles and proteins, thus maintaining cellular homeostasis.
Role in Cell Cycle and Apoptosis[edit | edit source]
TP53INP2 is induced by the tumor suppressor protein p53 in response to cellular stress. It can promote cell cycle arrest and apoptosis, thereby preventing the proliferation of damaged cells. This function is particularly important in the context of cancer, where TP53INP2 may act as a tumor suppressor.
Clinical Significance[edit | edit source]
Alterations in the expression of TP53INP2 have been associated with various diseases, including cancer and metabolic disorders. Overexpression of TP53INP2 has been observed in certain types of cancer, suggesting a potential role in tumorigenesis. Conversely, reduced expression of TP53INP2 has been linked to metabolic disorders such as obesity and diabetes.
Research Directions[edit | edit source]
Current research is focused on understanding the precise molecular mechanisms by which TP53INP2 regulates autophagy and its implications in disease. There is also interest in exploring TP53INP2 as a potential therapeutic target for cancer and metabolic diseases.
Also see[edit | edit source]
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Contributors: Prab R. Tumpati, MD