(Q43990741)

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Down-modulation of Bcl-XL, release of cytochrome c and sequential activation of caspases during honokiol-induced apoptosis in human squamous lung cancer CH27 cells

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Europe PubMed Central

PubMed publication ID

28 November 2017

Down-modulation of Bcl-XL, release of cytochrome c and sequential activation of caspases during honokiol-induced apoptosis in human squamous lung cancer CH27 cells (English)

1 reference

Europe PubMed Central

PubMed publication ID

28 November 2017

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Shu Er Yang

1

1 reference

Europe PubMed Central

PubMed publication ID

28 November 2017

Ming Tsuen Hsieh

2

1 reference

Europe PubMed Central

PubMed publication ID

28 November 2017

Tung Hu Tsai

3

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Europe PubMed Central

PubMed publication ID

28 November 2017

Shih Lan Hsu

4

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Europe PubMed Central

PubMed publication ID

28 November 2017

language of work or name

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publication date

1 May 2002

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Europe PubMed Central

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28 November 2017

Biochemical Pharmacology

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Europe PubMed Central

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28 November 2017

63

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Europe PubMed Central

PubMed publication ID

28 November 2017

9

1 reference

Europe PubMed Central

PubMed publication ID

28 November 2017

1641-1651

1 reference

Europe PubMed Central

PubMed publication ID

28 November 2017

Studies on the Components of Magnolia obovata THUNB. II. On the Components of the Methanol Extract of the Bark

1 reference

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7 January 2021

Identification and determination of honokiol and magnolol from Magnolia officinalis by high-performance liquid chromatography with phtodiode-array UV detection

1 reference

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7 January 2021

Magnolol and honokiol isolated from Magnolia officinalis protect rat heart mitochondria against lipid peroxidation

1 reference

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Two antiplatelet agents from Magnolia officinalis.

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Antimicrobial Activity of Phenolic Constituents of Magnolia Grandiflora L

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Pharmacological properties of magnolol and honokiol extracted from Magnolia officinalis: central depressant effects

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7 January 2021

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Studies on Inhibitors of Skin Tumor Promotion, IX. Neolignans from Magnolia officinalis

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Natural flavonoids and lignans are potent cytostatic agents against human leukemic HL-60 cells

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Apoptosis in the pathogenesis and treatment of disease

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Mechanisms and Functions of Cell Death

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The genetics of programmed cell death in the nematode Caenorhabditis elegans.

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Bcl-2-family proteins: the role of the BH3 domain in apoptosis

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Caenorhabditis elegans gene ced-9 protects cells from programmed cell death

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Bcl-2 and Bax function independently to regulate cell death

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Bax-independent inhibition of apoptosis by Bcl-XL.

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Caspases: killer proteases

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Caspases: the executioners of apoptosis

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Proteases to die for

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A license to kill

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Molecular ordering of the Fas-apoptotic pathway: the Fas/APO-1 protease Mch5 is a CrmA-inhibitable protease that activates multiple Ced-3/ICE-like cysteine proteases

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Caspase structure, proteolytic substrates, and function during apoptotic cell death

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The release of cytochrome c from mitochondria: a primary site for Bcl-2 regulation of apoptosis

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Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3

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Mitochondrial control of cell death

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Induction of apoptotic program in cell-free extracts: requirement for dATP and cytochrome c

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Cytochrome c-dependent and -independent induction of apoptosis in multiple myeloma cells

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Distinct stages of cytochrome c release from mitochondria: evidence for a feedback amplification loop linking caspase activation to mitochondrial dysfunction in genotoxic stress induced apoptosis

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Autocrine production of extracellular catalase prevents apoptosis of the human CEM T-cell line in serum-free medium

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A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding

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Cell Death in Development

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In vitro activation of CPP32 and Mch3 by Mch4, a novel human apoptotic cysteine protease containing two FADD-like domains

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Requirement for ceramide-initiated SAPK/JNK signalling in stress-induced apoptosis.

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Anti-apoptotic versus pro-apoptotic signal transduction: checkpoints and stop signs along the road to death.

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Ordering of ceramide formation, caspase activation, and mitochondrial changes during CD95- and DNA damage-induced apoptosis

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Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death

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Bad is a BH3 domain-containing protein that forms an inactivating dimer with Bcl-XL.

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Role for Bcl-xL as an inhibitor of cytosolic cytochrome C accumulation in DNA damage-induced apoptosis

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Identification of immunosuppressant-induced apoptosis in a murine B-cell line and its prevention by bcl-x but not bcl-2.

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Prevention of hypoxia-induced cell death by Bcl-2 and Bcl-xL.

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Bcl-XL interacts with Apaf-1 and inhibits Apaf-1-dependent caspase-9 activation

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Interaction of CED-4 with CED-3 and CED-9: a molecular framework for cell death

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Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization.

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Mitochondrial release of caspase-2 and -9 during the apoptotic process

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The central executioner of apoptosis: multiple connections between protease activation and mitochondria in Fas/APO-1/CD95- and ceramide-induced apoptosis

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Distinct caspase cascades are initiated in receptor-mediated and chemical-induced apoptosis.

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3-m-bromoacetylamino benzoic acid ethyl ester: a new cancericidal agent that activates the apoptotic pathway through caspase-9.

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DNA-damaging carcinogen 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) induces apoptosis via caspase-9 in primary cultured rat hepatocytes

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Involvement of the CD95 (APO–1/Fas) receptor/ligand system in drug–induced apoptosis in leukemia cells

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Drug-induced apoptosis in hepatoma cells is mediated by the CD95 (APO-1/Fas) receptor/ligand system and involves activation of wild-type p53.

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FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis

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

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T cells from baxalpha transgenic mice show accelerated apoptosis in response to stimuli but do not show restored DNA damage-induced cell death in the absence of p53.

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Identifiers

10.1016/S0006-2952(02)00894-8

1 reference

Europe PubMed Central

PubMed publication ID

28 November 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

28 November 2017

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