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Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked (1997)

J. Yang ; X. Liu ; K. Bhalla ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 275(5303): 1129-32.

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Publication Date: 1997-02-21

Description: Bcl-2 is an integral membrane protein located mainly on the outer membrane of mitochondria. Overexpression of Bcl-2 prevents cells from undergoing apoptosis in response to a variety of stimuli. Cytosolic cytochrome c is necessary for the initiation of the apoptotic program, suggesting a possible connection between Bcl-2 and cytochrome c, which is normally located in the mitochondrial intermembrane space. Cells undergoing apoptosis were found to have an elevation of cytochrome c in the cytosol and a corresponding decrease in the mitochondria. Overexpression of Bcl-2 prevented the efflux of cytochrome c from the mitochondria and the initiation of apoptosis. Thus, one possible role of Bcl-2 in prevention of apoptosis is to block cytochrome c release from mitochondria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, J -- Liu, X -- Bhalla, K -- Kim, C N -- Ibrado, A M -- Cai, J -- Peng, T I -- Jones, D P -- Wang, X -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1129-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9027314" target="_blank"〉PubMed〈/a〉

Keywords: Apoproteins/metabolism ; *Apoptosis ; Caspase 3 ; *Caspases ; Cysteine Endopeptidases/metabolism ; Cytochrome c Group/*metabolism ; Cytochromes c ; Cytosol/metabolism ; DNA Fragmentation ; Enzyme Activation ; Etoposide/pharmacology ; HL-60 Cells ; HeLa Cells ; Humans ; Intracellular Membranes/metabolism ; Membrane Potentials/drug effects ; Mitochondria/*metabolism ; Poly(ADP-ribose) Polymerases/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics/*metabolism ; Staurosporine/pharmacology ; Transfection

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

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A Crohn's disease variant in Atg16l1 enhances its degradation by caspase 3 (2014)

A. Murthy ; Y. Li ; I. Peng ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 506(7489): 456-62. doi: 10.1038/nature13044.

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Publication Date: 2014-02-21

Description: Crohn's disease is a debilitating inflammatory bowel disease (IBD) that can involve the entire digestive tract. A single-nucleotide polymorphism (SNP) encoding a missense variant in the autophagy gene ATG16L1 (rs2241880, Thr300Ala) is strongly associated with the incidence of Crohn's disease. Numerous studies have demonstrated the effect of ATG16L1 deletion or deficiency; however, the molecular consequences of the Thr300Ala (T300A) variant remains unknown. Here we show that amino acids 296-299 constitute a caspase cleavage motif in ATG16L1 and that the T300A variant (T316A in mice) significantly increases ATG16L1 sensitization to caspase-3-mediated processing. We observed that death-receptor activation or starvation-induced metabolic stress in human and murine macrophages increased degradation of the T300A or T316A variants of ATG16L1, respectively, resulting in diminished autophagy. Knock-in mice harbouring the T316A variant showed defective clearance of the ileal pathogen Yersinia enterocolitica and an elevated inflammatory cytokine response. In turn, deletion of the caspase-3-encoding gene, Casp3, or elimination of the caspase cleavage site by site-directed mutagenesis rescued starvation-induced autophagy and pathogen clearance, respectively. These findings demonstrate that caspase 3 activation in the presence of a common risk allele leads to accelerated degradation of ATG16L1, placing cellular stress, apoptotic stimuli and impaired autophagy in a unified pathway that predisposes to Crohn's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murthy, Aditya -- Li, Yun -- Peng, Ivan -- Reichelt, Mike -- Katakam, Anand Kumar -- Noubade, Rajkumar -- Roose-Girma, Merone -- DeVoss, Jason -- Diehl, Lauri -- Graham, Robert R -- van Lookeren Campagne, Menno -- England -- Nature. 2014 Feb 27;506(7489):456-62. doi: 10.1038/nature13044. Epub 2014 Feb 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Pathology, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Molecular Biology, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; ITGR Human Genetics, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24553140" target="_blank"〉PubMed〈/a〉

Keywords: Amino Acid Motifs ; Animals ; Autophagy/genetics ; Carrier Proteins/chemistry/*genetics/*metabolism ; Caspase 3/deficiency/genetics/*metabolism ; Cell Line ; Cells, Cultured ; Crohn Disease/*genetics/pathology ; Cytokines/immunology ; Enzyme Activation ; Female ; Food Deprivation ; Humans ; Macrophages/immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mutagenesis, Site-Directed ; Polymorphism, Single Nucleotide/*genetics ; *Proteolysis ; Stress, Physiological ; Yersinia enterocolitica/immunology

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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NRROS negatively regulates reactive oxygen species during host defence and autoimmunity (2014)

R. Noubade ; K. Wong ; N. Ota ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 509(7499): 235-9. doi: 10.1038/nature13152.

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Publication Date: 2014-04-18

Description: Reactive oxygen species (ROS) produced by phagocytes are essential for host defence against bacterial and fungal infections. Individuals with defective ROS production machinery develop chronic granulomatous disease. Conversely, excessive ROS can cause collateral tissue damage during inflammatory processes and therefore needs to be tightly regulated. Here we describe a protein, we termed negative regulator of ROS (NRROS), which limits ROS generation by phagocytes during inflammatory responses. NRROS expression in phagocytes can be repressed by inflammatory signals. NRROS-deficient phagocytes produce increased ROS upon inflammatory challenges, and mice lacking NRROS in their phagocytes show enhanced bactericidal activity against Escherichia coli and Listeria monocytogenes. Conversely, these mice develop severe experimental autoimmune encephalomyelitis owing to oxidative tissue damage in the central nervous system. Mechanistically, NRROS is localized to the endoplasmic reticulum, where it directly interacts with nascent NOX2 (also known as gp91(phox) and encoded by Cybb) monomer, one of the membrane-bound subunits of the NADPH oxidase complex, and facilitates the degradation of NOX2 through the endoplasmic-reticulum-associated degradation pathway. Thus, NRROS provides a hitherto undefined mechanism for regulating ROS production--one that enables phagocytes to produce higher amounts of ROS, if required to control invading pathogens, while minimizing unwanted collateral tissue damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noubade, Rajkumar -- Wong, Kit -- Ota, Naruhisa -- Rutz, Sascha -- Eidenschenk, Celine -- Valdez, Patricia A -- Ding, Jiabing -- Peng, Ivan -- Sebrell, Andrew -- Caplazi, Patrick -- DeVoss, Jason -- Soriano, Robert H -- Sai, Tao -- Lu, Rongze -- Modrusan, Zora -- Hackney, Jason -- Ouyang, Wenjun -- England -- Nature. 2014 May 8;509(7499):235-9. doi: 10.1038/nature13152. Epub 2014 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Immunology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA [2] Flexus Biosciences, 75 Shoreway Road, Suite D, San Carlos, California 94070, USA (R.N.); American Society for Biochemistry and Molecular Biology, 11200 Rockville Pike, Suite 302, Rockville, Maryland 20852, USA (P.A.V.). ; Department of Immunology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Antibody Engineering, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Pathology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Molecular Biology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Bioinformatics, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24739962" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Autoimmunity/genetics ; Bone Marrow Cells/cytology ; Central Nervous System/metabolism/pathology ; Encephalomyelitis, Autoimmune, Experimental/*immunology/*metabolism/pathology ; Endoplasmic Reticulum/enzymology/metabolism ; Escherichia coli/*immunology ; Female ; Inflammation/immunology/metabolism/pathology ; Listeria monocytogenes/*immunology ; Macrophages/cytology/enzymology/immunology/metabolism ; Male ; Mice ; NADPH Oxidase/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Phagocytes/cytology/immunology/metabolism ; Proteins/genetics/*metabolism ; Reactive Oxygen Species/*antagonists & inhibitors/metabolism

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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Probing the ultimate plasmon confinement limits with a van der Waals heterostructure (2018)

Alcaraz Iranzo, D., Nanot, S., Dias, E. J. C., Epstein, I., Peng, C., Efetov, D. K., Lundeberg, M. B., Parret, R., Osmond, J., Hong, J.-Y., Kong, J., Englund, D. R., Peres, N. M. R., Koppens, F. H. L.

American Association for the Advancement of Science (AAAS)

In: Science

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Publication Date: 2018-04-20

Description: The ability to confine light into tiny spatial dimensions is important for applications such as microscopy, sensing, and nanoscale lasers. Although plasmons offer an appealing avenue to confine light, Landau damping in metals imposes a trade-off between optical field confinement and losses. We show that a graphene-insulator-metal heterostructure can overcome that trade-off, and demonstrate plasmon confinement down to the ultimate limit of the length scale of one atom. This is achieved through far-field excitation of plasmon modes squeezed into an atomically thin hexagonal boron nitride dielectric spacer between graphene and metal rods. A theoretical model that takes into account the nonlocal optical response of both graphene and metal is used to describe the results. These ultraconfined plasmonic modes, addressed with far-field light excitation, enable a route to new regimes of ultrastrong light-matter interactions.

Keywords: Physics

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

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Characterisation of the novel spontaneously immortalized and invasively growing human skin keratinocyte line HaSKpw (2020)

Pavez Lorie, Elizabeth ; Stricker, Nicola ; Plitta-Michalak, Beata ; [et al.]

Springer Nature

In: Scientific Reports. 2020; 10(1): 15196. Published 2020 Sep 16. doi: 10.1038/s41598-020-71315-0.

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Publication Date: 2020-09-16

Description: We here present the spontaneously immortalised cell line, HaSKpw, as a novel model for the multistep process of skin carcinogenesis. HaSKpw cells were established from the epidermis of normal human adult skin that, without crisis, are now growing unrestricted and feeder-independent. At passage 22, clonal populations were established and clone7 (HaSKpwC7) was further compared to the also spontaneously immortalized HaCaT cells. As important differences, the HaSKpw cells express wild-type p53, remain pseudodiploid, and show a unique chromosomal profile with numerous complex aberrations involving chromosome 20. In addition, HaSKpw cells overexpress a pattern of genes and miRNAs such as KRT34, LOX, S100A9, miR21, and miR155; all pointing to a tumorigenic status. In concordance, HaSKpw cells exhibit reduced desmosomal contacts that provide them with increased motility and a highly migratory/invasive phenotype as demonstrated in scratch- and Boyden chamber assays. In 3D organotypic cultures, both HaCaT and HaSKpw cells form disorganized epithelia but only the HaSKpw cells show tumorcell-like invasive growth. Together, HaSKpwC7 and HaCaT cells represent two spontaneous (non-genetically engineered) “premalignant” keratinocyte lines from adult human skin that display different stages of the multistep process of skin carcinogenesis and thus represent unique models for analysing skin cancer development and progression.

Electronic ISSN: 2045-2322

Topics: Natural Sciences in General

Published by Springer Nature

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