Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis.

By Eri Oda, Rieko Ohki, H. Murasawa, J. Nemoto, T. Shibue, T. Yamashita, T. Tokino, Tadatsugu Taniguchi, N. Tanaka. Science, 2000

2,214 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/4b56fff1ae14c328af2d29ce3c6d4a4c0f8545ae

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In Cell Biology

1. Jerry M. Adams
2. K. Nakano
3. Junying Yuan
4. Douglas R. Green
5. W. Zong
6. Susan A. Elmore
7. Karen H. Vousden
8. Craig B. Thompson

In Molecular Biology

1. Jerry M. Adams
2. Douglas R. Green
3. A. Letai
4. Guido Kroemer
5. Suzanne Cory
6. A. Strasser
7. J. Chipuk
8. Simone Fulda

In Oncology

1. Jerry M. Adams
2. A. Strasser
3. Douglas R. Green
4. Simone Fulda
5. Suzanne Cory
6. B. Zhivotovsky
7. A. Letai
8. Karen H. Vousden

Citations in the corpus

• Apoptosis: A Review of Programmed Cell Death (2007, background): “Studies show that this protein can localize to the mitochondria and interact with anti-apoptotic Bcl-2 family members, resulting in the activation of caspase-9 (Oda et al., 2000).”
• p63 and p73 are required for p53-dependent apoptosis in response to DNA damage (2002, methodology): “Additionally, the NOXA promoter was used as another example of a p53 target gene believed to be important for p53 -dependent apoptosis”
• Hierarchical regulation of mitochondrion-dependent apoptosis by BCL-2 subfamilies (2006, background): “Interestingly, it seems that most, and probably all, intrinsic death signals activate both activator and inactivator BH3s simultaneously: DNA damage upregulates PUMA and NOX”
• Mitochondria in cancer cells: what is so special about them? (2008, positive): “p53 regulates the expression of the BH3-only proteins, p53 upregulated modulator of apoptosis (PUMA) and Noxa (Latin for damage), which promote OMM permeabilization during apoptosis [66, 67 ].”
• Apoptosis - the p53 network (2003, background): “Another p53 target gene,Noxa, contains a single p53responsive element in its promoter and is induced in response to X-ray irradiation (Oda et al., 2000).”
• Cellular and molecular mechanisms of mitochondrial function (2012, background): “68,69 The apoptogenic proteins can further be classi fi ed by the amount of Bcl-2 homology domains they contain.”
• Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics. (2002, background): “Multidomain proapoptotic proteins such as BAX and BAK tivity for multidomain BCL-2 members (Boyd et al., 1995; O’Connor et al., 1998; Oda et al., 2000; Wang et al., 1996; Yang etupon receipt of death signals participate in executing mitochon- drial dysfunction.”
• Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies (2016, background): “Moreover, p53 appears to promote the convergence of the intrinsic and extrinsic pathways through Bid regulation.”