The novel retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphtalene carboxylic acid can trigger apoptosis through a mitochondrial pathway independent of the nucleus.

No abstract is available for this paper.

• Publication year

  1999

• Venue

  Cancer Research

• Publication date

  1999-12-15

• Fields of study

  Biology, Medicine, Chemistry

• Identifiers
  PMID 10626821
• 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.

• Mitochondrial Permeability Transition

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  2001cited by this paper
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• Molecular characterization of mitochondrial apoptosis-inducing factor

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• Overexpression of bcl-2 or bcl-XL fails to inhibit apoptosis mediated by a novel retinoid.

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• Dihydroheptaprenyl and dihydrodecaprenyl monophosphates induce apoptosis mediated by activation of caspase-3-like protease.

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• Evidence for the involvement of both retinoic acid receptor- and retinoic X receptor-dependent signaling pathways in the induction of tissue transglutaminase and apoptosis in the human myeloma cell line RPMI 8226.

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• Activation of Mitochondria and Release of Mitochondrial Apoptogenic Factors by Betulinic Acid*

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• Growth-inhibitory effects of the synthetic retinoid CD437 against ovarian carcinoma models in vitro and in vivo

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• Induction of apoptosis by the novel retinoid AHPN in human T-cell lymphoma cells involves caspase-dependent and independent pathways

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• Selective Activation of an Apoptotic Retinoid Precursor in Macrophage Cell Lines*

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• The mitochondrial permeability transition.

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