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Article ; Online: Cleaning House: Selective Autophagy of Organelles.

Anding, Allyson L / Baehrecke, Eric H

2017 Volume 41, Issue 1, Page(s) 10–22

Abstract: The selective clearance of organelles by autophagy is critical for the regulation of cellular homeostasis in organisms from yeast to humans. Removal of damaged organelles clears the cell of potentially toxic byproducts and enables reuse of organelle ... ...

Abstract	The selective clearance of organelles by autophagy is critical for the regulation of cellular homeostasis in organisms from yeast to humans. Removal of damaged organelles clears the cell of potentially toxic byproducts and enables reuse of organelle components for bioenergetics. Thus, defects in organelle clearance may be detrimental to the health of the cells, contributing to cancer, neurodegeneration, and inflammatory diseases. Organelle-specific autophagy can clear mitochondria, peroxisomes, lysosomes, ER, chloroplasts, and the nucleus. Here, we review our understanding of the mechanisms that regulate the clearance of organelles by autophagy and highlight gaps in our knowledge of these processes.
MeSH term(s)	Animals ; Autophagy ; Humans ; Mitochondrial Degradation ; Models, Biological ; Organelles/metabolism
Language	English
Publishing date	2017-04-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2017.02.016
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Zs.A 5742: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 76: Show issues

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Article ; Online: Autophagy in Cell Life and Cell Death.

Anding, Allyson L / Baehrecke, Eric H

Current topics in developmental biology

2015 Volume 114, Page(s) 67–91

Abstract: Macroautophagy (hereafter referred to as autophagy) is a process used by the cell to deliver cytoplasmic components to the lysosome for degradation. Autophagy is most often associated with cell survival, as it provides cells with molecular building ... ...

Abstract	Macroautophagy (hereafter referred to as autophagy) is a process used by the cell to deliver cytoplasmic components to the lysosome for degradation. Autophagy is most often associated with cell survival, as it provides cells with molecular building blocks during periods of nutrient deprivation and also aids in the elimination of damaged organelles and protein aggregates. However, autophagy has also been implicated in cell death. Here, we review what is known about autophagy, its regulation, its role both in cell life and cell death, and what is known about autophagic cell death in vivo.
MeSH term(s)	Animals ; Apoptosis/physiology ; Autophagy/physiology ; Caenorhabditis elegans/cytology ; Caenorhabditis elegans/physiology ; Cell Death/physiology ; Cell Survival ; Dictyostelium/cytology ; Dictyostelium/physiology ; Drosophila melanogaster/cytology ; Drosophila melanogaster/physiology ; Starvation ; Vertebrates/physiology
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	1557-8933 ; 0070-2153
ISSN (online)	1557-8933
ISSN	0070-2153
DOI	10.1016/bs.ctdb.2015.07.012
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Article ; Online: 4-HPR Is an Endoplasmic Reticulum Stress Aggravator and Sensitizes Breast Cancer Cells Resistant to TRAIL/Apo2L.

Anding, Allyson L / Jones, James D / Newton, Michael A / Curley, Robert W / Clagett-Dame, Margaret

Anticancer research

2018 Volume 38, Issue 8, Page(s) 4403–4416

Abstract: Background/aim: N-(4-hydroxyphenyl)retinamide (4-HPR) is a synthetic retinoid, less toxic than the parent all-trans retinoic acid (RA). Unlike RA, 4-HPR induces apoptosis in tumor cells. Because 4-HPR can hydrolyze to liberate RA, a potent human ... ...

Abstract	Background/aim: N-(4-hydroxyphenyl)retinamide (4-HPR) is a synthetic retinoid, less toxic than the parent all-trans retinoic acid (RA). Unlike RA, 4-HPR induces apoptosis in tumor cells. Because 4-HPR can hydrolyze to liberate RA, a potent human teratogen, the unhydrolyzable ketone analog of 4-HPR, 4-hydroxybenzylretinone (4-HBR) has been prepared and has been found to cause apoptosis in tumor cells and shrink carcinogen-induced rat mammary tumors as 4-HPR does. Herein, we examined the mechanism whereby 4-HPR and 4-HBR induce apoptosis and death in breast cancer cells. Materials and methods: Gene expression profiling was conducted in MCF-7 cells over a 1.5- to 6-h time course and changes were validated by quantitative polymerase chain reaction (qPCR). Growth arrest and DNA damage-inducible protein 153 (GADD153 or C/EBP homologous protein, CHOP) was knocked down and the effect on 4-HPR-induced cell death and gene expression was assessed. 4-HPR synergy with tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL or Apo2 ligand) was also examined. Results: Drug treatment induced increased expression of endoplasmic reticulum (ER) stress-related and pro-apoptotic genes. Gene expression changes were verified by qPCR in three invasive ductal breast carcinoma cell lines (MCF-7, T-47D, MDA-MB-231). GADD153 showed the largest increase in the microarray experiment; however, knockdown of GADD153 did not abrogate apoptosis and death. Genes related to the extrinsic pathway of apoptosis including a receptor for TRAIL, death receptor 5 (DR5), were up-regulated by drug treatment. A dose of 4-HPR that alone is ineffective in killing TRAIL-resistant MCF-7 cells, synergized with recombinant TRAIL to induce breast cancer cell death. Conclusion: 4-HPR and analogs might be useful in sensitizing tumor cells to death receptor agonists.
MeSH term(s)	Apoptosis/drug effects ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Cell Death/drug effects ; Cell Division/drug effects ; Cell Line, Tumor ; Endoplasmic Reticulum Stress/drug effects ; Female ; Fenretinide/pharmacology ; Humans ; MCF-7 Cells ; Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism ; TNF-Related Apoptosis-Inducing Ligand/metabolism ; Transcription Factor CHOP/metabolism ; Tretinoin/metabolism ; Up-Regulation/drug effects
Chemical Substances	Receptors, TNF-Related Apoptosis-Inducing Ligand ; TNF-Related Apoptosis-Inducing Ligand ; TNFSF10 protein, human ; Transcription Factor CHOP (147336-12-7) ; Fenretinide (187EJ7QEXL) ; Tretinoin (5688UTC01R)
Language	English
Publishing date	2018-08
Publishing country	Greece
Document type	Journal Article
ZDB-ID	604549-2
ISSN	1791-7530 ; 0250-7005
ISSN (online)	1791-7530
ISSN	0250-7005
DOI	10.21873/anticanres.12742
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Zs.A 1642: Show issues

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Article ; Online: Vps13D Encodes a Ubiquitin-Binding Protein that Is Required for the Regulation of Mitochondrial Size and Clearance.

Anding, Allyson L / Wang, Chunxin / Chang, Tsun-Kai / Sliter, Danielle A / Powers, Christine M / Hofmann, Kay / Youle, Richard J / Baehrecke, Eric H

Current biology : CB

2018 Volume 28, Issue 2, Page(s) 287–295.e6

Abstract: The clearance of mitochondria by autophagy, mitophagy, is important for cell and organism health [1], and known to be regulated by ubiquitin. During Drosophila intestine development, cells undergo a dramatic reduction in cell size and clearance of ... ...

Abstract	The clearance of mitochondria by autophagy, mitophagy, is important for cell and organism health [1], and known to be regulated by ubiquitin. During Drosophila intestine development, cells undergo a dramatic reduction in cell size and clearance of mitochondria that depends on autophagy, the E1 ubiquitin-activating enzyme Uba1, and ubiquitin [2]. Here we screen a collection of putative ubiquitin-binding domain-encoding genes for cell size reduction and autophagy phenotypes. We identify the endosomal sorting complex required for transport (ESCRT) components TSG101 and Vps36, as well as the novel gene Vps13D. Vps13D is an essential gene that is necessary for autophagy, mitochondrial size, and mitochondrial clearance in Drosophila. Interestingly, a similar mitochondrial phenotype is observed in VPS13D mutant human cells. The ubiquitin-associated (UBA) domain of Vps13D binds K63 ubiquitin chains, and mutants lacking the UBA domain have defects in mitochondrial size and clearance and exhibit semi-lethality, highlighting the importance of Vps13D ubiquitin binding in both mitochondrial health and development. VPS13D mutant cells possess phosphorylated DRP1 and mitochondrial fission factor (MFF) as well as DRP1 association with mitochondria, suggesting that VPS13D functions downstream of these known regulators of mitochondrial fission. In addition, the large Vps13D mitochondrial and cell size phenotypes are suppressed by decreased mitochondrial fusion gene function. Thus, these results provide a previously unknown link between ubiquitin, mitochondrial size regulation, and autophagy.
MeSH term(s)	Animals ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Drosophila melanogaster/genetics ; Drosophila melanogaster/physiology ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Mitochondria/physiology ; Mitochondrial Size/genetics ; Mitophagy/genetics ; Ubiquitin/metabolism ; Ubiquitination
Chemical Substances	Carrier Proteins ; Drosophila Proteins ; Intracellular Signaling Peptides and Proteins ; Ubiquitin ; Vps13D protein, Drosophila
Language	English
Publishing date	2018-01-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2017.11.064
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Zs.A 3208: Show issues

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Article: Analysis of three variable number terminal repeat loci is sufficient to characterize the deoxyribonucleic acid fingerprints of a panel of human tumor cell lines.

Anding, Allyson L / Reiss, Tanika / Germain, Glen S

In vitro cellular & developmental biology. Animal

2003 Volume 39, Issue 7, Page(s) 273–274

Abstract: Using primers for the MCT118, YNZ22, and COL2A1 loci in polymerase chain reaction analysis we could distinguish among the approximately 20 cell lines routinely maintained in our laboratory. We also demonstrated that the cell line NB-1691 (a neuroblastoma) ...

Abstract	Using primers for the MCT118, YNZ22, and COL2A1 loci in polymerase chain reaction analysis we could distinguish among the approximately 20 cell lines routinely maintained in our laboratory. We also demonstrated that the cell line NB-1691 (a neuroblastoma) and its xenograft had an identical number of repeats at two loci. Rh30 (a rhabdomyosarcoma) made resistant to rapamycin was identical to its parent line and to a subline that had reverted to sensitivity after it was cultured without rapamycin in the medium.
MeSH term(s)	Base Sequence ; Cell Line, Tumor ; DNA Fingerprinting ; DNA Primers ; Humans ; Minisatellite Repeats ; Terminal Repeat Sequences
Chemical Substances	DNA Primers
Language	English
Publishing date	2003-07
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1077810-x
ISSN	1543-706X ; 1071-2690 ; 0883-8364
ISSN (online)	1543-706X
ISSN	1071-2690 ; 0883-8364
DOI	10.1290/1543-706X(2003)039<0273:AOTVNT>2.0.CO;2
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Zs.A 851: Show issues

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Article ; Online: 4-Hydroxybenzyl modification of the highly teratogenic retinoid, 4-[(1E)-2-(5,5,8,8-tetramethyl-5,6,7,8-tetrahydro-2-naphthalenyl)-1-propen-1-yl]benzoic acid (TTNPB), yields a compound that induces apoptosis in breast cancer cells and shows reduced teratogenicity.

Anding, Allyson L / Nieves, Nirca J / Abzianidze, Victoria V / Collins, Michael D / Curley, Robert W / Clagett-Dame, Margaret

Chemical research in toxicology

2011 Volume 24, Issue 11, Page(s) 1853–1861

Abstract: Retinoids are a class of compounds with structural similarity to vitamin A. These compounds inhibit the proliferation of many cancer cell lines but have had limited medical application as they are often toxic at therapeutic levels. Efforts to synthesize ... ...

Abstract	Retinoids are a class of compounds with structural similarity to vitamin A. These compounds inhibit the proliferation of many cancer cell lines but have had limited medical application as they are often toxic at therapeutic levels. Efforts to synthesize retinoids with a greater therapeutic index have met with limited success. 4-[(1E)-2-(5,5,8,8-tetramethyl-5,6,7,8-tetrahydro-2-naphthalenyl)-1-propen-1-yl]benzoic acid (TTNPB) is one of the most biologically active all-trans-retinoic acid (atRA) analogues and is highly teratogenic. In this study, we show that modification of the TTNPB carboxyl group with an N-(4-hydroxyphenyl)amido (4HPTTNPB) or a 4-hydroxybenzyl (4HBTTNPB) group changes the activity of the compound in cell culture and in vivo. Unlike TTNPB, both compounds induce apoptosis in cancer cells and bind poorly to the retinoic acid receptors (RARs). Like the similarly modified all-trans-retinoic acid (atRA) analogues N-(4-hydroxyphenyl)retinamide (4-HPR/fenretinide) and 4-hydroxybenzylretinone (4-HBR), 4HBTTNPB is a potent activator of components of the ER stress pathway. The amide-linked analogue, 4HPTTNPB, is less toxic to developing embryos than the parent TTNPB, and most significantly, the 4-hydroxybenzyl-modified compound (4HBTTNPB) that cannot be hydrolyzed in vivo to the parent TTNPB compound is nearly devoid of teratogenic liability.
MeSH term(s)	Administration, Oral ; Amides/chemistry ; Animals ; Antineoplastic Agents/adverse effects ; Antineoplastic Agents/chemical synthesis ; Antineoplastic Agents/therapeutic use ; Apoptosis/drug effects ; Benzoates/adverse effects ; Benzoates/chemical synthesis ; Benzoates/therapeutic use ; Binding, Competitive ; Breast Neoplasms/drug therapy ; Breast Neoplasms/pathology ; Cell Division/drug effects ; Cell Line, Tumor ; Endoplasmic Reticulum/drug effects ; Endoplasmic Reticulum/metabolism ; Female ; Fenretinide/chemical synthesis ; Fenretinide/therapeutic use ; Humans ; Phenol/chemistry ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Receptors, Retinoic Acid/metabolism ; Retinoids/adverse effects ; Retinoids/chemical synthesis ; Retinoids/therapeutic use ; Teratogens ; Transcription Factor CHOP/biosynthesis ; Vitamin A/analogs & derivatives ; Vitamin A/chemical synthesis ; Vitamin A/therapeutic use
Chemical Substances	4-hydroxybenzylretinone ; Amides ; Antineoplastic Agents ; Benzoates ; DDIT3 protein, human ; Receptors, Retinoic Acid ; Retinoids ; Teratogens ; Vitamin A (11103-57-4) ; Transcription Factor CHOP (147336-12-7) ; Fenretinide (187EJ7QEXL) ; Phenol (339NCG44TV) ; 4-(2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-1-propenyl)benzoic acid (71441-28-6)
Language	English
Publishing date	2011-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639353-6
ISSN	1520-5010 ; 0893-228X
ISSN (online)	1520-5010
ISSN	0893-228X
DOI	10.1021/tx200174n
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Zs.A 2320: Show issues

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Article: The unhydrolyzable fenretinide analogue 4-hydroxybenzylretinone induces the proapoptotic genes GADD153 (CHOP) and Bcl-2-binding component 3 (PUMA) and apoptosis that is caspase- dependent and independent of the retinoic acid receptor.

Anding, Allyson L / Chapman, Jason S / Barnett, Derek W / Curley, Robert W / Clagett-Dame, Margaret

Cancer research

2007 Volume 67, Issue 13, Page(s) 6270–6277

Abstract: The synthetic retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) induces apoptosis in a variety of cell lines and has shown promise as an anticancer agent both in vitro and in vivo. The clinical dose of 4-HPR, however, is limited by residual-associated ... ...

Abstract	The synthetic retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) induces apoptosis in a variety of cell lines and has shown promise as an anticancer agent both in vitro and in vivo. The clinical dose of 4-HPR, however, is limited by residual-associated toxicities, indicating a need for a less toxic drug. In this study, we show that 4-hydroxybenzylretinone (4-HBR), the unhydrolyzable analogue of 4-HPR, is effective in producing apoptosis in a variety of 4-HPR-sensitive cell lines, including breast cancer, neuroblastoma, and leukemia cells. We also show through the use of a pan-caspase inhibitor that this 4-HBR-induced apoptosis is dependent, at least in part, on caspase activity. 4-HBR is shown to exhibit binding to the retinoic acid receptors (RAR) at concentrations necessary to induce cell death and induces expression of all-trans-retinoic acid-responsive genes that can be blocked by a RAR pan-antagonist. However, through the use of this RAR pan-antagonist, 4-HBR-induced apoptosis and cell death is shown to be independent of the RAR signaling pathway. To further characterize the mechanism of action of 4-HBR, expression of the endoplasmic reticulum stress-induced genes GADD153 and Bcl-2-binding component 3 was examined. These mRNAs are shown to be rapidly induced in 4-HBR-treated and 4-HPR-treated breast cancer cells, and this up-regulation is also shown to be independent of the RARs. These results suggest that a stress-mediated apoptotic cascade is involved in the mechanism of action of these retinoids.
MeSH term(s)	Apoptosis ; Apoptosis Regulatory Proteins/biosynthesis ; Caspases/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Fenretinide/analogs & derivatives ; HL-60 Cells ; Humans ; Hydrolysis ; Leukemia/metabolism ; Proto-Oncogene Proteins/biosynthesis ; RNA, Messenger/metabolism ; Receptors, Retinoic Acid/metabolism ; Retinoids/metabolism ; Transcription Factor CHOP/biosynthesis ; Vitamin A/analogs & derivatives ; Vitamin A/pharmacology
Chemical Substances	4-hydroxybenzylretinone ; Apoptosis Regulatory Proteins ; BBC3 protein, human ; Proto-Oncogene Proteins ; RNA, Messenger ; Receptors, Retinoic Acid ; Retinoids ; Vitamin A (11103-57-4) ; Transcription Factor CHOP (147336-12-7) ; Fenretinide (187EJ7QEXL) ; Caspases (EC 3.4.22.-)
Language	English
Publishing date	2007-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-07-0727
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Article: Solid phase-assisted synthesis and screening of a small library of N-(4-hydroxyphenyl)retinamide (4-HPR) analogs.

Mershon, Serena M / Anding, Allyson L / Chapman, Jason S / Clagett-Dame, Margaret / Stonerock, Laura A / Curley, Robert W

Bioorganic & medicinal chemistry letters

2007 Volume 17, Issue 3, Page(s) 836–840

Abstract: Using solid phase-assisted synthesis and purification, a 49 member library of analogs of the mammary tumor chemopreventive retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) has been prepared. After prescreening for growth inhibitory activity in human ... ...

Abstract	Using solid phase-assisted synthesis and purification, a 49 member library of analogs of the mammary tumor chemopreventive retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) has been prepared. After prescreening for growth inhibitory activity in human mammary tumor cells (MCF-7) in culture, most of those analogs which showed activity (12 of them) were assayed for apoptosis-inducing activity in the MCF-7 cells. At least 3 of the analogs (13, 24, and 28) showed activity approaching that of 4-HPR.
MeSH term(s)	Antineoplastic Agents/chemical synthesis ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Breast Neoplasms/drug therapy ; Cell Line, Tumor ; Chromatography, High Pressure Liquid ; Drug Screening Assays, Antitumor ; Fenretinide/analogs & derivatives ; Fenretinide/chemical synthesis ; Fenretinide/pharmacology ; Humans ; In Situ Nick-End Labeling
Chemical Substances	Antineoplastic Agents ; Fenretinide (187EJ7QEXL)
Language	English
Publishing date	2007-02-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1063195-1
ISSN	1464-3405 ; 0960-894X
ISSN (online)	1464-3405
ISSN	0960-894X
DOI	10.1016/j.bmcl.2006.10.050
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