Inhibiting BTB domain and CNC homolog 1 (Bach1) as an alternative to increase Nrf2 activation in chronic diseases-Reference-Cited by-同舟云学术

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Inhibiting BTB domain and CNC homolog 1 (Bach1) as an alternative to increase Nrf2 activation in chronic diseases

Published:2022-06 Issue:6 Volume:1866 Page:130129
ISSN:0304-4165
Container-title:Biochimica et Biophysica Acta (BBA) - General Subjects
language:en
Short-container-title:Biochimica et Biophysica Acta (BBA) - General Subjects

Author:

Mafra Denise,Alvarenga Livia,Cardozo Ludmila F.M.F.,Stockler-Pinto Milena B.,Nakao Lia S.,Stenvinkel Peter,Shiels Paul G.

Funder

Conselho Nacional de Desenvolvimento Científico e Tecnológico

Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro

Publisher

Elsevier BV

Subject

Molecular Biology,Biochemistry,Biophysics

Reference115 articles.

1. Bach1: function, regulation, and involvement in disease;Zhang;Oxidative Med. Cell. Longev.,2018

2. Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus;Sheng;FEBS Open Bio.,2020

3. The critical role of Bach2 in shaping the balance between CD4+ T cell subsets in immune-mediated diseases;Yang;Mediat. Inflamm.,2019

4. Bach1 represses Wnt/β-catenin signaling and angiogenesis;Jiang;Circ. Res.,2015

5. Bach1 induces endothelial cell apoptosis and cell-cycle arrest through ROS generation;Wang;Oxidative Med. Cell. Longev.,2016

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