Deletion of MCL-1 causes lethal cardiac failure and mitochondrial dysfunction. - Wikidata - wikimedia - TriplyDB

Deletion of MCL-1 causes lethal cardiac failure and mitochondrial dysfunction.

Deletion of MCL-1 causes lethal cardiac failure and mitochondrial dysfunction.

http://www.wikidata.org/entity/Q36981764

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The Role of Cardiolipin in Cardiovascular Health The two faces of miR-29 Recent advances in mitochondrial research Regulation of cardiac expression of the diabetic marker microRNA miR-29 A Maltose-Binding Protein Fusion Construct Yields a Robust Crystallography Platform for MCL1 Differential Effects of β-Blockers, Angiotensin II Receptor Blockers, and a Novel AT2R Agonist NP-6A4 on Stress Response of Nutrient-Starved Cardiovascular Cells Inhibition of miR-302 Suppresses Hypoxia-Reoxygenation-Induced H9c2 Cardiomyocyte Death by Regulating Mcl-1 Expression Mcl-1 ubiquitination: unique regulation of an essential survival protein.Maritoclax induces apoptosis in acute myeloid leukemia cells with elevated Mcl-1 expression Potent and selective small-molecule MCL-1 inhibitors demonstrate on-target cancer cell killing activity as single agents and in combination with ABT-263 (navitoclax).Cardiac-Specific SOCS3 Deletion Prevents In Vivo Myocardial Ischemia Reperfusion Injury through Sustained Activation of Cardioprotective Signaling Molecules.Allosteric inhibition of antiapoptotic MCL-1.Cyclin E/Cdk2-dependent phosphorylation of Mcl-1 determines its stability and cellular sensitivity to BH3 mimetics Mcl-1 is a key regulator of the ovarian reserve Attacking cancer's Achilles heel: antagonism of anti-apoptotic BCL-2 family members MicroRNA-128 inhibition attenuates myocardial ischemia/reperfusion injury-induced cardiomyocyte apoptosis by the targeted activation of peroxisome proliferator-activated receptor gamma.Targeting of MCL-1 kills MYC-driven mouse and human lymphomas even when they bear mutations in p53 Many players in BCL-2 family affairs.Lessons from gain- and loss-of-function models of pro-survival Bcl2 family proteins: implications for targeted therapy.Mitochondrial apoptosis: killing cancer using the enemy within.Regulation of mitochondrial nutrient and energy metabolism by BCL-2 family proteins.Emerging understanding of Bcl-2 biology: Implications for neoplastic progression and treatment.Targeting skeletal muscle mitochondria to prevent type 2 diabetes in youth.A novel chalcone derivative S17 induces apoptosis through ROS dependent DR5 up-regulation in gastric cancer cells.Non-apoptotic functions of BCL-2 family proteins.Directly targeting the mitochondrial pathway of apoptosis for cancer therapy using BH3 mimetics - recent successes, current challenges and future promise.EGF-mediated induction of Mcl-1 at the switch to lactation is essential for alveolar cell survival.Survival control of malignant lymphocytes by anti-apoptotic MCL-1.Myeloid-derived suppressor activity is mediated by monocytic lineages maintained by continuous inhibition of extrinsic and intrinsic death pathways.Therapeutic inhibition of BCL-2 and related family members.Amsacrine-induced apoptosis of human leukemia U937 cells is mediated by the inhibition of AKT- and ERK-induced stabilization of MCL1.Re-activation of mitochondrial apoptosis inhibits T-cell lymphoma survival and treatment resistance.Endothelial cell survival during angiogenesis requires the pro-survival protein MCL1 Loss of MCL-1 leads to impaired autophagy and rapid development of heart failure.Mcl-1 regulates reactive oxygen species via NOX4 during chemotherapy-induced senescence.VCP cooperates with UBXD1 to degrade mitochondrial outer membrane protein MCL1 in model of Huntington's disease.Voruciclib, a clinical stage oral CDK9 inhibitor, represses MCL-1 and sensitizes high-risk Diffuse Large B-cell Lymphoma to BCL2 inhibition.Anti-apoptotic BCL-2 family members in development.Why do BCL-2 inhibitors work and where should we use them in the clinic?Developmental Regulation of Mitochondrial Apoptosis by c-Myc Governs Age- and Tissue-Specific Sensitivity to Cancer Therapeutics.

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Deletion of MCL-1 causes lethal cardiac failure and mitochondrial dysfunction.

http://www.wikidata.org/entity/Q36981764

description

2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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2013年论文

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2013年论文

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name

Deletion of MCL-1 causes lethal cardiac failure and mitochondrial dysfunction.

@en

type

label

Deletion of MCL-1 causes lethal cardiac failure and mitochondrial dysfunction.

@en

prefLabel

Deletion of MCL-1 causes lethal cardiac failure and mitochondrial dysfunction.

@en

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Genes & Development

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Deletion of MCL-1 causes lethal cardiac failure and mitochondrial dysfunction.

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Brian Koss

http://www.w3.org/2001/XMLSchema#string

Christopher Calabrese

http://www.w3.org/2001/XMLSchema#string

Jerold E Rehg

http://www.w3.org/2001/XMLSchema#string

John D Schuetz

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John Lynch

http://www.w3.org/2001/XMLSchema#string

Joseph T Opferman

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Madhavi Bathina

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Sharon Frase

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Xi Wang

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P2860

Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak

Mechanisms of apoptosis sensitivity and resistance to the BH3 mimetic ABT-737 in acute myeloid leukemia

MCL-1 is a stress sensor that regulates autophagy in a developmentally regulated manner

The intracellular distribution and pattern of expression of Mcl-1 overlap with, but are not identical to, those of Bcl-2

Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members

Mitochondria and mitophagy: the yin and yang of cell death control

BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis

Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death

Ischemic preconditioning reduces apoptosis by upregulating anti-death gene Bcl-2

Bax regulates primary necrosis through mitochondrial dynamics

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1351-1364

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10.1101/GAD.215855.113

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12

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27

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240309950

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23788622

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3701191

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