MOAP-1 Mediates Fas-Induced Apoptosis in Liver by Facilitating tBid Recruitment to Mitochondria

Tan, Chong Teik; Zhou, Qiling; Su, Y. K.; Fu, Nai Yang; Chang, Hao‐Chun; Tao, Ran; Sukumaran, Sunil K.; Baksh, Shairaz; Tan, Yee-Joo; Sabapathy, Kanaga; Yu, Chundong; Yu, Victor C.

doi:10.1016/j.celrep.2016.05.068

Cited by 27 publications

(48 citation statements)

References 49 publications

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“…However, there is no reported unusual/abnormal phenotype in MOAP-1 −/− mice. It has been noted that these mice develop normally to adulthood and are fertile [5]. In our hands, they do not appear to differ significantly from MOAP-1 +/+ mice in appearance, body weight (Fig.…”

Section: Introductionsupporting

confidence: 46%

“…All animal procedures were carried out with approval and oversight from the Institutional Animal Care and Use Committee (IACUC) of the National University of Singapore and conducted in compliance with the National Advisory Committee for Laboratory Animal Research (NACLAR) guidelines. MOAP-1 −/− mice were developed as previously described [5]. Briefly, the targeting vector was designed to replace the entire coding region of MOAP-1 exon 2 gene with the neomycin cassette via homologous recombination.…”

Section: Methodsmentioning

confidence: 99%

“…It is suggested that MOAP-1, like RASSF1A, is itself a tumor suppressor protein [4]. MOAP-1 also mediates Fas-induced apoptosis in the liver and MOAP-1 −/− mice are protected from Fas apoptotic signaling-induced acute liver injury [5]. However, there is no reported unusual/abnormal phenotype in MOAP-1 −/− mice.…”

Section: Introductionmentioning

confidence: 99%

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Absence of Stress Response in Dorsal Raphe Nucleus in Modulator of Apoptosis 1-Deficient Mice

et al. 2018

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Modulator of apoptosis 1 (MOAP-1) is a Bcl-2-associated X Protein (BAX)-associating protein that plays an important role in regulating apoptosis. It is highly enriched in the brain but its function in this organ remains unknown. Studies on BAX mice suggested that disruption of programmed cell death may lead to abnormal emotional states. We thus hypothesize that MOAP-1 mice may also display stress-related behavioral differences and perhaps involved in stress responses in the brain and investigated if a depression-like trait exists in MOAP-1 mice, and if so, whether it is age related, and how it relates to central serotonergic stress response in the dorsal raphe nucleus. Young MOAP-1 mice exhibit depression-like behavior, in the form of increased immobility time when compared to age-matched wild-type mice in the forced swimming test, which is abolished by acute treatment of fluoxetine. This is supported by data from the tail suspension and sucrose preference tests. Repeated forced swimming stress causes an up-regulation of tryptophan hydroxylase 2 (TPH2) and a down-regulation of brain-derived neurotrophic factor (BDNF) in the dorsal raphe nucleus (DRN) in young wild-type (WT) control mice. In contrast, TPH2 up-regulation was not observed in aged WT mice. Interestingly, such a stress response appears absent in both young and aged MOAP-1 mice. Aged MOAP-1 and WT mice also have similar immobility times on the forced swimming test. These data suggest that MOAP-1 is required in the regulation of stress response in the DRN. Crosstalk between BDNF and 5-HT appears to play an important role in this stress response.

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Section: Introductionsupporting

confidence: 46%

Section: Methodsmentioning

confidence: 99%

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Absence of Stress Response in Dorsal Raphe Nucleus in Modulator of Apoptosis 1-Deficient Mice

et al. 2018

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“…Conversely, in “type II cells” (e.g., hepatocytes, pancreatic β cells, and a majority of cancer cells), in which CASP3 and CASP7 activation is restrained by XIAP [ 310 ], extrinsic apoptosis requires the proteolytic cleavage of BID by CASP8 [ 70 , 311 , 312 ]. This leads to the generation of a truncated form of BID (tBID), which translocates to the OMM [ 313 , 314 ] via a mechanism that, at least upon FAS stimulation, reportedly depends on the binding of modulator of apoptosis 1 (MOAP1) to the alleged BID receptor mitochondrial carrier 2 (MTCH2) [ 315 , 316 ]. At the OMM, tBID operates as a BH3-only activator to engage BAX/BAK-dependent MOMP-driven and consequent CASP9-driven RCD.…”

Section: Extrinsic Apoptosismentioning

confidence: 99%

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

et al. 2018

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Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

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“…exposed BH3-like domain to interact and promote Bax activation, leading to transmigration of activated Bax to the mitochondria[30,85,86]. Other than RASSF1A, MOAP-1 was reported as MTCH2 interacting protein and plays an important role in Fas receptor mediated apoptosis signalling by promoting recruitment of tBid to the mitochondria during apoptosis[87].…”

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confidence: 99%

PNMA family: Protein interaction network and cell signalling pathways implicated in cancer and apoptosis

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et al. 2018

Cellular Signalling

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Paraneoplastic Ma Family (PNMA) comprises a growing number of family members which share relatively conserved protein sequences encoded by the human genome and is localized to several human chromosomes, including the X-chromosome. Based on sequence analysis, PNMA family members share sequence homology to the Gag protein of LTR retrotransposon, and several family members with aberrant protein expressions have been reported to be closely associated with the human Paraneoplastic Disorder (PND). In addition, gene mutations of specific members of PNMA family are known to be associated with human mental retardation or 3-M syndrome consisting of restrictive post-natal growth or dwarfism, and development of skeletal abnormalities. Other than sequence homology, the physiological function of many members in this family remains unclear. However, several members of this family have been characterized, including cell signalling events mediated by these proteins that are associated with apoptosis, and cancer in different cell types. Furthermore, while certain PNMA family members show restricted gene expression in the human brain and testis, other PNMA family members exhibit broader gene expression or preferential and selective protein interaction profiles, suggesting functional divergence within the family. Functional analysis of some members of this family have identified protein domains that are required for subcellular localization, protein-protein interactions, and cell signalling events which are the focus of this review paper.

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MOAP-1 Mediates Fas-Induced Apoptosis in Liver by Facilitating tBid Recruitment to Mitochondria

Cited by 27 publications

References 49 publications

Absence of Stress Response in Dorsal Raphe Nucleus in Modulator of Apoptosis 1-Deficient Mice

Absence of Stress Response in Dorsal Raphe Nucleus in Modulator of Apoptosis 1-Deficient Mice

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

PNMA family: Protein interaction network and cell signalling pathways implicated in cancer and apoptosis

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