Nuclear oncoprotein prothymosin alpha is a partner of Keap1: implications for expression of oxidative stress-protecting genes. - Wikidata - wikimedia - TriplyDB

Nuclear oncoprotein prothymosin alpha is a partner of Keap1: implications for expression of oxidative stress-protecting genes.

Nuclear oncoprotein prothymosin alpha is a partner of Keap1: implications for expression of oxidative stress-protecting genes.

http://www.wikidata.org/entity/Q40890652

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p62/SQSTM1 is a target gene for transcription factor NRF2 and creates a positive feedback loop by inducing antioxidant response element-driven gene transcription The Nrf2-antioxidant response element signaling pathway and its activation by oxidative stress Activation of Nrf2 by arsenite and monomethylarsonous acid is independent of Keap1-C151: enhanced Keap1-Cul3 interaction The inflammatory and normal transcriptome of mouse bladder detrusor and mucosa Concerted action of Nrf2-ARE pathway, MRN complex, HMGB1 and inflammatory cytokines - implication in modification of radiation damage Emerging functional cross-talk between the Keap1-Nrf2 system and mitochondria Regulation of Nrf2-Mediated Phase II Detoxification and Anti-oxidant Genes Microsecond molecular dynamics simulations of intrinsically disordered proteins involved in the oxidative stress response Novel -Propeller of the BTB-Kelch Protein Krp1 Provides a Binding Site for Lasp-1 That Is Necessary for Pseudopodial Extension Keap1 controls postinduction repression of the Nrf2-mediated antioxidant response by escorting nuclear export of Nrf2 PGAM5 tethers a ternary complex containing Keap1 and Nrf2 to mitochondria Stress-activated cap'n'collar transcription factors in aging and human disease Basic principles and emerging concepts in the redox control of transcription factors Antioxidant-induced modification of INrf2 cysteine 151 and PKC-delta-mediated phosphorylation of Nrf2 serine 40 are both required for stabilization and nuclear translocation of Nrf2 and increased drug resistance Inhibitor of Nrf2 (INrf2 or Keap1) protein degrades Bcl-xL via phosphoglycerate mutase 5 and controls cellular apoptosis Dysfunctional KEAP1-NRF2 interaction in non-small-cell lung cancer Nrf2 controls constitutive and inducible expression of ARE-driven genes through a dynamic pathway involving nucleocytoplasmic shuttling by Keap1 Dihydro-CDDO-trifluoroethyl amide (dh404), a novel Nrf2 activator, suppresses oxidative stress in cardiomyocytes.Quantitative proteomic analysis reveals the perturbation of multiple cellular pathways in HL-60 cells induced by arsenite treatment.Novel small molecules relieve prothymosin alpha-mediated inhibition of apoptosome formation by blocking its interaction with Apaf-1.Modifying specific cysteines of the electrophile-sensing human Keap1 protein is insufficient to disrupt binding to the Nrf2 domain Neh2 The ubiquitin-conjugating enzyme UbcM2 can regulate the stability and activity of the antioxidant transcription factor Nrf2.Pyrimidine biosynthesis links mitochondrial respiration to the p53 pathway.Nrf2 and Keap1 abnormalities in non-small cell lung carcinoma and association with clinicopathologic features.INrf2 (Keap1) targets Bcl-2 degradation and controls cellular apoptosis.Nrf2 is overexpressed in pancreatic cancer: implications for cell proliferation and therapy.Subcellular dissemination of prothymosin alpha at normal physiology: immunohistochemical vis-a-vis western blotting perspective Oxidant-induced cell death and Nrf2-dependent antioxidative response are controlled by Fra-1/AP-1 Non-electrophilic modulators of the canonical Keap1/Nrf2 pathway Multiple nuclear localization signals function in the nuclear import of the transcription factor Nrf2.Chemical and biological mechanisms of phytochemical activation of Nrf2 and importance in disease prevention Two-site substrate recognition model for the Keap1-Nrf2 system: a hinge and latch mechanism.Phosphorylation and dephosphorylation of tyrosine 141 regulate stability and degradation of INrf2: a novel mechanism in Nrf2 activation.Function of prothymosin alpha in chromatin decondensation and expression of thymosin beta-4 linked to angiogenesis and synaptic plasticity.The NRF2 activation and antioxidative response are not impaired overall during hyperoxia-induced lung epithelial cell death Prothymosin α overexpression contributes to the development of pulmonary emphysema.Immunocytological and preliminary immunohistochemical studies of prothymosin alpha, a human cancer-associated polypeptide, with a well-characterized polyclonal antibody.Molecular mechanisms of Nrf2-mediated antioxidant response Dual roles of Nrf2 in cancer.The Nrf2/ARE pathway as a potential therapeutic target in neurodegenerative disease.

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Nuclear oncoprotein prothymosin alpha is a partner of Keap1: implications for expression of oxidative stress-protecting genes.

http://www.wikidata.org/entity/Q40890652

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Nuclear oncoprotein prothymosi ...... ative stress-protecting genes.

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MCB.25.3.1089-1099.2005

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Molecular and Cellular Biology

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Nuclear oncoprotein prothymosi ...... dative stress-protecting genes

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Andrey B Vartapetian

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Elena A Sukhacheva

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Grigoriy S Filonov

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Irina S Abaeva

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Nina V Chichkova

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Ruben N Karapetian

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Ulrich Schneider

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Yuri P Rubtsov

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P2860

Nuclear distribution of prothymosin alpha and parathymosin: evidence that prothymosin alpha is associated with RNA synthesis processing and parathymosin with early DNA replication

HIP-I: a huntingtin interacting protein isolated by the yeast two-hybrid system

Prothymosin alpha interacts with the CREB-binding protein and potentiates transcription.

Prothymosin alpha selectively enhances estrogen receptor transcriptional activity by interacting with a repressor of estrogen receptor activity

Evidence for nuclear targeting of prothymosin and parathymosin synthesized in situ

Expression of alpha-thymosins in human tissues in normal and abnormal growth

Small Maf proteins serve as transcriptional cofactors for keratinocyte differentiation in the Keap1-Nrf2 regulatory pathway

Keap1 represses nuclear activation of antioxidant responsive elements by Nrf2 through binding to the amino-terminal Neh2 domain

The human prothymosin alpha gene is polymorphic and induced upon growth stimulation: evidence using a cloned cDNA

Nrf2 is a direct PERK substrate and effector of PERK-dependent cell survival

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1089-1099

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10.1128/MCB.25.3.1089-1099.2005

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3

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Sergey V Melnikov

Alexandra Evstafieva

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2005-02-01T00:00:00Z

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15657435

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