ArticleThe Journal of biological chemistry2012
Cytosolic Bax: does it require binding proteins to keep its pro-apoptotic activity in check?
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- The C-terminal sequences of Bcl-2 family proteins mediate interactions that regulate cell death.The Biochemical journal · 2024Review
- Chemical modulation of cytosolic BAX homodimer potentiates BAX activation and apoptosis.Nature communications · 2023Article
- Insect Peptide CopA3 Mitigates the Effects of Heat Stress on Porcine Muscle Satellite Cells.Animals : an open access journal from MDPI · 2023Article
- Potential Chemopreventive Role of Pterostilbene in Its Modulation of the Apoptosis Pathway.International journal of molecular sciences · 2023Review
- Loss of PKD1/polycystin-1 impairs lysosomal activity in a CAPN (calpain)-dependent manner.Autophagy · 2021Article
- EBV BCL-2 homologue BHRF1 drives chemoresistance and lymphomagenesis by inhibiting multiple cellular pro-apoptotic proteins.Cell death and differentiation · 2020Article
- An evolutionary perspective on the role of mesencephalic astrocyte-derived neurotrophic factor (MANF): At the crossroads of poriferan innate immune and apoptotic pathways.Biochemistry and biophysics reports · 2017Article
- Cytosolic Ku70 regulates Bax-mediated cell death.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- The porin VDAC2 is the mitochondrial platform for Bax retrotranslocation.Scientific reports · 2016Article
- An Autoinhibited Dimeric Form of BAX Regulates the BAX Activation Pathway.Molecular cell · 2016Article
- Bax targets mitochondria by distinct mechanisms before or during apoptotic cell death: a requirement for VDAC2 or Bak for efficient Bax apoptotic function.Cell death and differentiation · 2014Article
- Conformational rearrangements in the pro-apoptotic protein, Bax, as it inserts into mitochondria: a cellular death switch.The Journal of biological chemistry · 2014Article
- Building blocks of the apoptotic pore: how Bax and Bak are activated and oligomerize during apoptosis.Cell death and differentiation · 2014Review
- The apoptotic pore on mitochondria: are we breaking through or still stuck?Cell death and differentiation · 2014Article
- Identification of Bax-interacting proteins in oligodendrocyte progenitors during glutamate excitotoxicity and perinatal hypoxia-ischemia.ASN neuro · 2013Article
- Apoptosis induced by the fungal pathogen gliotoxin requires a triple phosphorylation of Bim by JNK.Cell death and differentiation · 2013Article
- Apoptosis of osteosarcoma cultures by the combination of the cyclin-dependent kinase inhibitor SCH727965 and a heat shock protein 90 inhibitor.Cell death & disease · 2013Article
- Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) protein-induced lysosomal translocation of proapoptotic effectors is mediated by phosphofurin acidic cluster sorting protein-2 (PACS-2).The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bax is kept inactive in the cytosol by refolding its C-terminal transmembrane domain into the hydrophobic binding pocket. Although energetic calculations predicted this conformation to be stable, numerous Bax binding proteins were reported and suggested to further stabilize inactive Bax. Unfortunately, most of them have not been validated in a physiological context on the endogenous level. Here we use gel filtration analysis of the cytosol of primary and established cells to show that endogenous, inactive Bax runs 20-30 kDa higher than recombinant Bax, suggesting Bax dimerization or the binding of a small protein. Dimerization was excluded by a lack of interaction of differentially tagged Bax proteins and by comparing the sizes of dimerized recombinant Bax with cytosolic Bax on blue native gels. Surprisingly, when analyzing cytosolic Bax complexes by high sensitivity mass spectrometry after anti-Bax immunoprecipitation or consecutive purification by gel filtration and blue native gel electrophoresis, we detected only one protein, called p23 hsp90 co-chaperone, which consistently and specifically co-purified with Bax. However, this protein could not be validated as a crucial inhibitory Bax binding partner as its over- or underexpression did not show any apoptosis defects. By contrast, cytosolic Bax exhibits a slight molecular mass shift on SDS-PAGE as compared with recombinant Bax, which suggests a posttranslational modification and/or a structural difference between the two proteins. We propose that in most healthy cells, cytosolic endogenous Bax is a monomeric protein that does not necessarily need a binding partner to keep its pro-apoptotic activity in check.
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