Bcl-2 family proteins and the regulation of programmed cell death in leukemia and lymphoma.

No abstract is available for this paper.

• Publication year

  1996

• Venue

  Cancer treatment and research

• Publication date

  Unknown publication date

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1007/978-1-4613-1261-1_3PMID 8724625
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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• Tumor suppressor p53 is a direct transcriptional activator of the human bax gene.

  1995cited by this paper
• Multiple Bcl-2 family members demonstrate selective dimerizations with Bax.

  1995cited by this paper
• bcl-2 deficiency in mice leads to pleiotropic abnormalities: accelerated lymphoid cell death in thymus and spleen, polycystic kidney, hair hypopigmentation, and distorted small intestine.

  1995cited by this paper
• The intracellular distribution and pattern of expression of Mcl-1 overlap with, but are not identical to, those of Bcl-2

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• Overexpression of Bcl-XL by cytotoxic drug exposure confers resistance to ionizing radiation-induced internucleosomal DNA fragmentation.

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• Induction of apoptosis by the Bcl-2 homologue Bak

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• Biochemical and functional comparisons of Mcl-1 and Bcl-2 proteins: evidence for a novel mechanism of regulating Bcl-2 family protein function.

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  1995cited by this paper
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  1994cited by this paper
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  1994cited by this paper
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• T and B memory cells.

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  1994cited by this paper
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