Deficiency of apoptosis-stimulating protein 2 of p53 protects mice from acute hepatic injury induced by CCl via autophagy.

08:00 EDT 9th September 2019 | BioPortfolio

Summary of "Deficiency of apoptosis-stimulating protein 2 of p53 protects mice from acute hepatic injury induced by CCl via autophagy."

Apoptosis-stimulating protein 2 of p53 (ASPP2) has a variety of biological functions, and is involved in cellular apoptosis, autophagy and inflammatory reaction. However, the role of ASPP2 in acute hepatic injury remains unclear.


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This article was published in the following journal.

Name: Toxicology letters
ISSN: 1879-3169


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Medical and Biotech [MESH] Definitions

An autosomal dominant disorder showing decreased levels of plasma protein S antigen or activity, associated with venous thrombosis and pulmonary embolism. PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C (also a vitamin K-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis. (From Harrison's Principles of Internal Medicine, 12th ed, p1511; Wintrobe's Clinical Hematology, 9th ed, p1523)

A nucleocytoplasmic transport protein that binds to ALPHA KARYOPHERINS and RAN GTP BINDING PROTEIN inside the CELL NUCLEUS and participates in their export into CYTOPLASM. It is also associated with the regulation of APOPTOSIS and microtubule assembly.

The vitamin K-dependent cofactor of activated PROTEIN C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S; (PROTEIN S DEFICIENCY); can lead to recurrent venous and arterial thrombosis.

A nutritional condition produced by a deficiency of proteins in the diet, characterized by adaptive enzyme changes in the liver, increase in amino acid synthetases, and diminution of urea formation, thus conserving nitrogen and reducing its loss in the urine. Growth, immune response, repair, and production of enzymes and hormones are all impaired in severe protein deficiency. Protein deficiency may also arise in the face of adequate protein intake if the protein is of poor quality (i.e., the content of one or more amino acids is inadequate and thus becomes the limiting factor in protein utilization). (From Merck Manual, 16th ed; Harrison's Principles of Internal Medicine, 12th ed, p406)

A BCL-2-like protein that has a C-terminal BCL-2 homology (BH3) domain and forms heterodimers with other BCL-2 FAMILY PROTEINS. It is a strong inducer of APOPTOSIS and ANOIKIS; several isoforms are expressed (BimEL, Bim L, Bim-alpha, Bim-s; and Bim-gamma) that have different potencies for inducing apoptosis.

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