Biological properties of the BCL-2 family protein BCL-RAMBO, which regulates apoptosis, mitochondrial fragmentation, and mitophagy

Kataoka, Takao

doi:10.3389/fcell.2022.1065702

Cited by 8 publications

(2 citation statements)

References 203 publications

(298 reference statements)

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“…BCL2L13 (BCL2-like 13, BCL-RAMBO) is an atypical member of the BCL2 family that regulates apoptosis, mitochondrial fragmentation, and mitophagy [95]. ACE2 stimulates the induction of browning in white adipose tissue [96], while the expression of BCL2L13 increases during white adipose tissue browning [97].…”

Section: Genes/proteins Identified By 1-l Transcription Of C-(aa)n-n ...mentioning

confidence: 99%

1-L Transcription of SARS-CoV-2 Spike Protein S1 Subunit

Nahalka

2024

IJMS

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The COVID-19 pandemic prompted rapid research on SARS-CoV-2 pathogenicity. Consequently, new data can be used to advance the molecular understanding of SARS-CoV-2 infection. The present bioinformatics study discusses the “spikeopathy” at the molecular level and focuses on the possible post-transcriptional regulation of the SARS-CoV-2 spike protein S1 subunit in the host cell/tissue. A theoretical protein–RNA recognition code was used to check the compatibility of the SARS-CoV-2 spike protein S1 subunit with mRNAs in the human transcriptome (1-L transcription). The principle for this method is elucidated on the defined RNA binding protein GEMIN5 (gem nuclear organelle-associated protein 5) and RNU2-1 (U2 spliceosomal RNA). Using the method described here, it was shown that 45% of the genes/proteins identified by 1-L transcription of the SARS-CoV-2 spike protein S1 subunit are directly linked to COVID-19, 39% are indirectly linked to COVID-19, and 16% cannot currently be associated with COVID-19. The identified genes/proteins are associated with stroke, diabetes, and cardiac injury.

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Section: Genes/proteins Identified By 1-l Transcription Of C-(aa)n-n ...mentioning

confidence: 99%

1-L Transcription of SARS-CoV-2 Spike Protein S1 Subunit

Nahalka

2024

IJMS

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“…BCL-RAMBO, also known as BCL2-like 13, was initially discovered as a pro-apoptotic protein 15 . Many studies have demonstrated that BCL-RAMBO controls cell death, mitochondria fragmentation, and mitophagy 16 , 17 . BCL-RAMBO consists of an N-terminal BH domain, a No BH (BHNo) domain, a transmembrane (TM) domain, and a short cytoplasmic tail 15 .…”

Section: Introductionmentioning

confidence: 99%

The BCL-2 family protein BCL-RAMBO interacts and cooperates with GRP75 to promote its apoptosis signaling pathway

Xu,

Hashino,

Tanaka

et al. 2023

Sci Rep

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The BCL-2 family protein BCL-RAMBO, also known as BCL2-like 13, anchors at the outer mitochondrial membrane and regulates apoptosis, mitochondrial fragmentation, and mitophagy. However, the mechanisms underlying the proapoptotic role of BCL-RAMBO remain unclear. In the present study, we demonstrated that BCL-RAMBO interacted with glucose-regulated protein 75 (GRP75), also known as heat shock protein family A member 9, and mortalin using co-immunoprecipitation and glutathione S-transferase-based pull-down assays. BCL-RAMBO interacted with GRP75 via its No BCL-2 homology domain. The interaction between BCL-RAMBO and GRP75 was confirmed by genetic interactions in Drosophila because a rough eye phenotype caused by the ectopic expression of BCL-RAMBO was partially suppressed by mutations in Hsc70-5, a mammalian GRP75 ortholog. In human embryonic kidney 293T cells, the co-expression of BCL-RAMBO and GRP75 facilitated an elevation in executioner caspase activity and poly (ADP-ribose) polymerase 1 (PARP-1) cleavage. In contrast, the knockdown of GRP75 suppressed elevated executioner caspase activity and PARP-1 cleavage in BCL-RAMBO-transfected cells. The mitochondrial release of cytochrome c induced by BCL-RAMBO was also attenuated by the knockdown of GRP75. These results indicate that GRP75 interacts with BCL-RAMBO and plays a crucial role in the BCL-RAMBO-dependent apoptosis signaling pathway.

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Molecular mechanism of autophagy and apoptosis in endometriosis: Current understanding and future research directions

Kobayashi,

Imanaka,

Yoshimoto

et al. 2024

Reprod Medicine & Biology

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BackgroundEndometriosis is a common gynecological condition, with symptoms including pain and infertility. Regurgitated endometrial cells into the peritoneal cavity encounter hypoxia and nutrient starvation. Endometriotic cells have evolved various adaptive mechanisms to survive in this inevitable condition. These adaptations include escape from apoptosis. Autophagy, a self‐degradation system, controls apoptosis during stress conditions. However, to date, the mechanisms regulating the interplay between autophagy and apoptosis are still poorly understood. In this review, we summarize the current understanding of the molecular characteristics of autophagy in endometriosis and discuss future therapeutic challenges.MethodsA search of PubMed and Google Scholar databases were used to identify relevant studies for this narrative literature review.ResultsAutophagy may be dynamically regulated through various intrinsic (e.g., PI3K/AKT/mTOR signal transduction network) and extrinsic (e.g., hypoxia and iron‐mediated oxidative stress) pathways, contributing to the development and progression of endometriosis. Upregulation of mTOR expression suppresses apoptosis via inhibiting the autophagy pathway, whereas hypoxia or excess iron often inhibits apoptosis via promoting autophagy.ConclusionEndometriotic cells may have acquired antiapoptotic mechanisms through unique intrinsic and extrinsic autophagy pathways to survive in changing environments.

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Biological properties of the BCL-2 family protein BCL-RAMBO, which regulates apoptosis, mitochondrial fragmentation, and mitophagy

Cited by 8 publications

References 203 publications

1-L Transcription of SARS-CoV-2 Spike Protein S1 Subunit

1-L Transcription of SARS-CoV-2 Spike Protein S1 Subunit

The BCL-2 family protein BCL-RAMBO interacts and cooperates with GRP75 to promote its apoptosis signaling pathway

Molecular mechanism of autophagy and apoptosis in endometriosis: Current understanding and future research directions

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