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Book ; Conference proceedings: Peroxisomes

Reddy, Janardan K.

biology and role in toxicology and disease ; [proceedings of the International Symposium on Peroxisomes held on June 28 - July 2, 1995, Aspen, Colorado]

(Annals of the New York Academy of Sciences ; 804)

1996

Event/congress	International Symposium on Peroxisomes (1995, AspenColo.)
Author's details	ed. by Janardan K. Reddy
Series title	Annals of the New York Academy of Sciences ; 804
Collection
Keywords	Peroxisomal Disorders / congresses ; Microbodies / congresses ; Neoplasms / etiology / congresses ; Peroxisom
Subject	Peroxysom
Language	English
Size	XV, 801 S. : Ill., graph. Darst.
Publishing place	New York, NY
Publishing country	United States
Document type	Book ; Conference proceedings
HBZ-ID	HT007474317
ISBN	0-89766-967-3 ; 0-89766-968-1 ; 978-0-89766-967-2 ; 978-0-89766-968-9
Database	Catalogue ZB MED Medicine, Health

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Se 110 -804-	verfügbar in Königswinter	Königswinter

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Book ; Conference proceedings: Peroxisomes

Reddy, Janardan K.

biology and role in toxicology and disease ; the Aspen Institute, Aspen, Colorado June June 28 - July 2, 1995

1995

Event/congress	International Symposium on Peroxisomes (1995, AspenColo.)
Author's details	International Symposium on Peroxisomes: Biology and Role in Toxicology and Diseaseed. [Organizers J. K. Reddy ...]
Keywords	Peroxisomal Disorders ; Microbodies ; Neoplasms / etiology
Language	English
Size	[234] Bl.
Publishing place	s.l.
Publishing country	United States
Document type	Book ; Conference proceedings
HBZ-ID	HT014240790
Database	Catalogue ZB MED Medicine, Health

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2004 A 5736	order for loan	Magazin

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Article ; Online: Trimethylguanosine synthase 1 is a novel regulator of pancreatic beta-cell mass and function.

Blandino-Rosano, Manuel / Romaguera Llacer, Pau / Lin, Ashley / Reddy, Janardan K / Bernal-Mizrachi, Ernesto

The Journal of biological chemistry

2022 Volume 298, Issue 3, Page(s) 101592

Abstract: Type 2 diabetes is a metabolic disorder associated with abnormal glucose homeostasis and is characterized by intrinsic defects in β-cell function and mass. Trimethylguanosine synthase 1 (TGS1) is an evolutionarily conserved enzyme that methylates small ... ...

Abstract	Type 2 diabetes is a metabolic disorder associated with abnormal glucose homeostasis and is characterized by intrinsic defects in β-cell function and mass. Trimethylguanosine synthase 1 (TGS1) is an evolutionarily conserved enzyme that methylates small nuclear and nucleolar RNAs and that is involved in pre-mRNA splicing, transcription, and ribosome production. However, the role of TGS1 in β-cells and glucose homeostasis had not been explored. Here, we show that TGS1 is upregulated by insulin and upregulated in islets of Langerhans from mice exposed to a high-fat diet and in human β-cells from type 2 diabetes donors. Using mice with conditional (βTGS1KO) and inducible (MIP-Cre
MeSH term(s)	Animals ; Diabetes Mellitus, Type 2/enzymology ; Diabetes Mellitus, Type 2/metabolism ; Glucose/metabolism ; Insulin/metabolism ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/enzymology ; Insulin-Secreting Cells/metabolism ; Methyltransferases/metabolism ; Mice ; Mice, Knockout
Chemical Substances	Insulin ; Methyltransferases (EC 2.1.1.-) ; trimethylguanosine synthase (EC 2.1.1.-) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-01-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2022.101592
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Article ; Online: Peroxisome proliferator-activated receptor-α activation and excess energy burning in hepatocarcinogenesis.

Misra, Parimal / Reddy, Janardan K

Biochimie

2014 Volume 98, Page(s) 63–74

Abstract: Peroxisome proliferator-activated receptor-α (PPARα) modulates the activities of all three interlinked hepatic fatty acid oxidation systems, namely mitochondrial and peroxisomal β-oxidation and microsomal ω-oxidation pathways. Hyperactivation of PPARα, ... ...

Abstract	Peroxisome proliferator-activated receptor-α (PPARα) modulates the activities of all three interlinked hepatic fatty acid oxidation systems, namely mitochondrial and peroxisomal β-oxidation and microsomal ω-oxidation pathways. Hyperactivation of PPARα, by both exogenous and endogenous activators up-regulates hepatic fatty acid oxidation resulting in excess energy burning in liver contributing to the development of liver cancer in rodents. Sustained PPARα signaling disproportionately increases H2O2-generating fatty acid metabolizing enzymes as compared to H2O2-degrading enzymes in liver leading to enhanced generation of DNA damaging reactive oxygen species, progressive endoplasmic reticulum stress and inflammation. These alterations also contribute to increased liver cell proliferation with changes in apoptosis. Thus, reactive oxygen species, oxidative stress and hepatocellular proliferation are likely the main contributing factors in the pathogenesis of hepatocarcinogenesis, mediated by sustained PPARα activation-related energy burning in liver. Furthermore, the transcriptional co-activator Med1, a key subunit of the Mediator complex, is essential for PPARα signaling in that both PPARα-null and Med1-null hepatocytes are unresponsive to PPARα activators and fail to give rise to liver tumors when chronically exposed to PPARα activators.
MeSH term(s)	Animals ; Cell Proliferation ; Energy Metabolism ; Fatty Acids/metabolism ; Liver/drug effects ; Liver/metabolism ; Liver Neoplasms/chemically induced ; Mediator Complex Subunit 1/physiology ; Mice ; Mice, Knockout ; MicroRNAs/physiology ; Oxidation-Reduction ; Oxidative Stress ; PPAR alpha/metabolism ; Peroxisome Proliferators/adverse effects ; Peroxisomes/physiology
Chemical Substances	Fatty Acids ; Med1 protein, mouse ; Mediator Complex Subunit 1 ; MicroRNAs ; PPAR alpha ; Peroxisome Proliferators
Language	English
Publishing date	2014-03
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	120345-9
ISSN	1638-6183 ; 0300-9084
ISSN (online)	1638-6183
ISSN	0300-9084
DOI	10.1016/j.biochi.2013.11.011
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Article ; Online: Nuclear receptors and transcription factors in the development of fatty liver disease.

Vluggens, Aurore / Reddy, Janardan K

Current drug metabolism

2012 Volume 13, Issue 10, Page(s) 1422–1435

Abstract: Liver regulates certain key aspects of lipid metabolism including de novo lipogenesis, fatty acid oxidation, and lipoprotein uptake and secretion. Disturbances in these hepatic functions can contribute to the development of fatty liver disease. An ... ...

Abstract	Liver regulates certain key aspects of lipid metabolism including de novo lipogenesis, fatty acid oxidation, and lipoprotein uptake and secretion. Disturbances in these hepatic functions can contribute to the development of fatty liver disease. An understanding of the regulatory mechanisms influencing hepatic lipid homeostasis and systemic energy balance is therefore of paramount importance in gaining insights that might be useful in the management of fatty liver disease. In this regard, emerging evidence indicates that certain members of the nuclear receptor superfamily and some key transcription coactivators function as intracellular sensors to orchestrate hepatic lipid metabolism. Dysregulation of nuclear receptor-mediated transcriptional signaling and perturbations in the levels of their cognate endogenous ligands play a prominent role in the development of fatty liver disease. The potential of nuclear receptors, transcription coactivators as well as enzymes that participate in the synthesis and degradation of endogenous nuclear receptor ligands, as effective therapeutic targets for fatty liver disease needs evaluation.
MeSH term(s)	Animals ; Fatty Liver/metabolism ; Humans ; Receptors, Cytoplasmic and Nuclear/metabolism ; Transcription Factors/metabolism
Chemical Substances	Receptors, Cytoplasmic and Nuclear ; Transcription Factors
Language	English
Publishing date	2012-10-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2064815-7
ISSN	1875-5453 ; 1389-2002
ISSN (online)	1875-5453
ISSN	1389-2002
DOI	10.2174/138920012803762710
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Article: Peroxisome proliferators and peroxisome proliferator-activated receptor alpha: biotic and xenobiotic sensing.

Reddy, Janardan K

The American journal of pathology

2004 Volume 164, Issue 6, Page(s) 2305–2321

MeSH term(s)	Adipose Tissue/physiology ; Animals ; Awards and Prizes ; Illinois ; Lipolysis/physiology ; Liver/cytology ; Mice ; Mice, Knockout ; Microbodies/physiology ; Microbodies/ultrastructure ; Oxidative Stress ; Pathology ; Peroxisome Proliferators ; Peroxisomes/physiology ; Peroxisomes/ultrastructure ; Receptors, Cytoplasmic and Nuclear/deficiency ; Receptors, Cytoplasmic and Nuclear/drug effects ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/physiology ; Transcription Factors/deficiency ; Transcription Factors/drug effects ; Transcription Factors/genetics ; Transcription Factors/physiology ; Xenobiotics/pharmacology
Chemical Substances	Peroxisome Proliferators ; Receptors, Cytoplasmic and Nuclear ; Transcription Factors ; Xenobiotics
Language	English
Publishing date	2004-05-21
Publishing country	United States
Document type	Lecture ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/s0002-9440(10)63787-x
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Article ; Online: Mouse Cardiac Pde1C Is a Direct Transcriptional Target of Pparα.

Shete, Varsha / Liu, Ning / Jia, Yuzhi / Viswakarma, Navin / Reddy, Janardan K / Thimmapaya, Bayar

International journal of molecular sciences

2018 Volume 19, Issue 12

Abstract: Phosphodiesterase 1C (PDE1C) is expressed in mammalian heart and regulates cardiac functions by controlling levels of second messenger cyclic AMP and cyclic GMP (cAMP and cGMP, respectively). However, molecular mechanisms of ... ...

Abstract	Phosphodiesterase 1C (PDE1C) is expressed in mammalian heart and regulates cardiac functions by controlling levels of second messenger cyclic AMP and cyclic GMP (cAMP and cGMP, respectively). However, molecular mechanisms of cardiac
MeSH term(s)	Animals ; Cell Line ; Cyclic AMP/metabolism ; Cyclic Nucleotide Phosphodiesterases, Type 1/genetics ; Cyclic Nucleotide Phosphodiesterases, Type 1/metabolism ; Mediator Complex Subunit 1/genetics ; Mediator Complex Subunit 1/metabolism ; Mice ; Mice, Inbred C57BL ; Myocardium/metabolism ; PPAR alpha/genetics ; PPAR alpha/metabolism ; Promoter Regions, Genetic ; Protein Binding ; Transcriptional Activation
Chemical Substances	Med1 protein, mouse ; Mediator Complex Subunit 1 ; PPAR alpha ; Cyclic AMP (E0399OZS9N) ; Cyclic Nucleotide Phosphodiesterases, Type 1 (EC 3.1.4.17) ; Pde1C protein, mouse (EC 3.1.4.17)
Language	English
Publishing date	2018-11-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19123704
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Article: Med1 subunit of the mediator complex in nuclear receptor-regulated energy metabolism, liver regeneration, and hepatocarcinogenesis.

Jia, Yuzhi / Viswakarma, Navin / Reddy, Janardan K

Gene expression

2014 Volume 16, Issue 2, Page(s) 63–75

Abstract: Several nuclear receptors regulate diverse metabolic functions that impact on critical biological processes, such as development, differentiation, cellular regeneration, and neoplastic conversion. In the liver, some members of the nuclear receptor family, ...

Abstract	Several nuclear receptors regulate diverse metabolic functions that impact on critical biological processes, such as development, differentiation, cellular regeneration, and neoplastic conversion. In the liver, some members of the nuclear receptor family, such as peroxisome proliferator-activated receptors (PPARs), constitutive androstane receptor (CAR), farnesoid X receptor (FXR), liver X receptor (LXR), pregnane X receptor (PXR), glucocorticoid receptor (GR), and others, regulate energy homeostasis, the formation and excretion of bile acids, and detoxification of xenobiotics. Excess energy burning resulting from increases in fatty acid oxidation systems in liver generates reactive oxygen species, and the resulting oxidative damage influences liver regeneration and liver tumor development. These nuclear receptors are important sensors of exogenous activators as well as receptor-specific endogenous ligands. In this regard, gene knockout mouse models revealed that some lipid-metabolizing enzymes generate PPARα-activating ligands, while others such as ACOX1 (fatty acyl-CoA oxidase1) inactivate these endogenous PPARα activators. In the absence of ACOX1, the unmetabolized ACOX1 substrates cause sustained activation of PPARα, and the resulting increase in energy burning leads to hepatocarcinogenesis. Ligand-activated nuclear receptors recruit the multisubunit Mediator complex for RNA polymerase II-dependent gene transcription. Evidence indicates that the Med1 subunit of the Mediator is essential for PPARα, PPARγ, CAR, and GR signaling in liver. Med1 null hepatocytes fail to respond to PPARα activators in that these cells do not show induction of peroxisome proliferation and increases in fatty acid oxidation enzymes. Med1-deficient hepatocytes show no increase in cell proliferation and do not give rise to liver tumors. Identification of nuclear receptor-specific coactivators and Mediator subunits should further our understanding of the complexities of metabolic diseases associated with increased energy combustion in liver.
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Energy Metabolism ; Humans ; Liver Regeneration ; Mediator Complex Subunit 1/genetics ; Mediator Complex Subunit 1/physiology ; Receptors, Cytoplasmic and Nuclear/metabolism
Chemical Substances	MED1 protein, human ; Mediator Complex Subunit 1 ; Receptors, Cytoplasmic and Nuclear
Language	English
Publishing date	2014-05-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1151108-4
ISSN	1052-2166 ; 1052-2116
ISSN	1052-2166 ; 1052-2116
DOI	10.3727/105221614X13919976902219
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Article ; Online: Med1 regulates meiotic progression during spermatogenesis in mice.

Huszar, Jessica M / Jia, Yuzhi / Reddy, Janardan K / Payne, Christopher J

Reproduction (Cambridge, England)

2015 Volume 149, Issue 6, Page(s) 597–604

Abstract: Spermatogenesis is a highly coordinated process. Signaling from nuclear hormone receptors, like those for retinoic acid (RA), is important for normal spermatogenesis. However, the mechanisms regulating these signals are poorly understood. Mediator ... ...

Abstract	Spermatogenesis is a highly coordinated process. Signaling from nuclear hormone receptors, like those for retinoic acid (RA), is important for normal spermatogenesis. However, the mechanisms regulating these signals are poorly understood. Mediator complex subunit 1 (MED1) is a transcriptional enhancer that directly modulates transcription from nuclear hormone receptors. MED1 is present in male germ cells throughout mammalian development, but its function during spermatogenesis is unknown. To determine its role, we generated mice lacking Med1 specifically in their germ cells beginning just before birth. Conditional Med1 knockout males are fertile, exhibiting normal testis weights and siring ordinary numbers of offspring. RA-responsive gene products stimulated by RA gene 8 (Stra8) and synaptonemal complex protein 3 (Sycp3) are first detected in knockout spermatogonia at the expected time points during the first wave of spermatogenesis, and persist with normal patterns of cellular distribution in adult knockout testes. Meiotic progression, however, is altered in the absence of Med1. At postnatal day 7 (P7), zygotene-stage knockout spermatocytes are already detected, unlike in control testes, with fewer pre-leptotene-stage cells and more leptotene spermatocytes observed in the knockouts. At P9, Med1 knockout spermatocytes prematurely enter pachynema. Once formed, greater numbers of knockout spermatocytes remain in pachynema relative to the other stages of meiosis throughout testis development and its maintenance in the adult. Meiotic exit is not inhibited. We conclude that MED1 regulates the temporal progression of primary spermatocytes through meiosis, with its absence resulting in abbreviated pre-leptotene, leptotene, and zygotene stages, and a prolonged pachytene stage.
MeSH term(s)	Animals ; Male ; Mediator Complex Subunit 1/genetics ; Mediator Complex Subunit 1/metabolism ; Meiosis/genetics ; Mice ; Mice, Knockout ; Pachytene Stage/genetics ; Spermatogenesis/genetics ; Testis/metabolism
Chemical Substances	Med1 protein, mouse ; Mediator Complex Subunit 1
Language	English
Publishing date	2015-03-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2034501-X
ISSN	1741-7899 ; 1470-1626 ; 1476-3990
ISSN (online)	1741-7899
ISSN	1470-1626 ; 1476-3990
DOI	10.1530/REP-14-0483
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Article: Peroxisome proliferator-activated receptor-α signaling in hepatocarcinogenesis.

Misra, Parimal / Viswakarma, Navin / Reddy, Janardan K

Sub-cellular biochemistry

2013 Volume 69, Page(s) 77–99

Abstract: Peroxisomes are subcellular organelles that are found in the cytoplasm of most animal cells. They perform diverse metabolic functions, including H2O2-derived respiration, β-oxidation of fatty acids, and cholesterol metabolism. Peroxisome proliferators ... ...

Abstract	Peroxisomes are subcellular organelles that are found in the cytoplasm of most animal cells. They perform diverse metabolic functions, including H2O2-derived respiration, β-oxidation of fatty acids, and cholesterol metabolism. Peroxisome proliferators are a large class of structurally dissimilar industrial and pharmaceutical chemicals that were originally identified as inducers of both the size and the number of peroxisomes in rat and mouse livers or hepatocytes in vitro. Exposure to peroxisome proliferators leads to a stereotypical orchestration of adaptations consisting of hepatocellular hypertrophy and hyperplasia, and transcriptional induction of fatty acid metabolizing enzymes regulated in parallel with peroxisome proliferation. Chronic exposure to peroxisome proliferators causes liver tumors in both male and female mice and rats. Evidence indicates a pivotal role for a subset of nuclear receptor superfamily members, called peroxisome proliferator-activated receptors (PPARs), in mediating energy metabolism. Upon activation, PPARs regulate the expression of genes involved in lipid metabolism and peroxisome proliferation, as well as genes involved in cell growth. In this review, we describe the molecular mode of action of PPAR transcription factors, including ligand binding, interaction with specific DNA response elements, transcriptional activation, and cross talk with other signaling pathways. We discuss the evidence that suggests that PPARα and transcriptional coactivator Med1/PBP, a key subunit of the Mediator complex play a central role in mediating hepatic steatosis to hepatocarcinogenesis. Disproportionate increases in H2O2-generating enzymes generates excess reactive oxygen species resulting in sustained oxidative stress and progressive endoplasmic reticulum (ER) stress with activation of unfolded protein response signaling. Thus, these major contributors coupled with hepatocellular proliferation are the key players of peroxisome proliferators-induced hepatocarcinogenesis.
MeSH term(s)	Animals ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Energy Metabolism ; Fatty Acids/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Liver/metabolism ; Liver/pathology ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Mice ; Mice, Knockout ; Oxidation-Reduction ; PPAR alpha/metabolism ; Peroxisomes/metabolism ; Peroxisomes/pathology ; Signal Transduction
Chemical Substances	Fatty Acids ; PPAR alpha
Language	English
Publishing date	2013
Publishing country	United States
Document type	Journal Article ; Review
ISSN	0306-0225 ; 0096-8757
ISSN	0306-0225 ; 0096-8757
DOI	10.1007/978-94-007-6889-5_5
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