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Article ; Online: Galectin-3 in NAFLD: Therapeutic Target or Noncausal Biomarker?

Soccio, Raymond E

The Journal of clinical endocrinology and metabolism

2021 Volume 106, Issue 9, Page(s) e3773–e3774

MeSH term(s)	Biomarkers ; Galectin 3 ; Humans ; Mendelian Randomization Analysis ; Non-alcoholic Fatty Liver Disease/drug therapy
Chemical Substances	Biomarkers ; Galectin 3
Language	English
Publishing date	2021-05-19
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgab363
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Article: Pparγ1

Jiao, Xuanmao / Tian, Lifeng / Zhang, Zhao / Balcerek, Joanna / Kossenkov, Andrew V / Casimiro, Mathew C / Wang, Chenguang / Liu, Yichuan / Ertel, Adam / Soccio, Raymond E / Chen, Eric R / Liu, Qin / Ashton, Anthony W / Tong, Wei / Pestell, Richard G

Cancers

2021 Volume 13, Issue 9

Abstract: HER2, which is associated with clinically aggressive disease, is overexpressed in 15-20% of breast cancers (BC). The host immune system participates in the therapeutic response of ... ...

Abstract	HER2, which is associated with clinically aggressive disease, is overexpressed in 15-20% of breast cancers (BC). The host immune system participates in the therapeutic response of HER2
Language	English
Publishing date	2021-04-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13092171
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Thiazolidinediones and the promise of insulin sensitization in type 2 diabetes.

Soccio, Raymond E / Chen, Eric R / Lazar, Mitchell A

Cell metabolism

2014 Volume 20, Issue 4, Page(s) 573–591

Abstract: Type 2 diabetes is caused by insulin resistance coupled with an inability to produce enough insulin to control blood glucose, and thiazolidinediones (TZDs) are the only current antidiabetic agents that function primarily by increasing insulin sensitivity. ...

Abstract	Type 2 diabetes is caused by insulin resistance coupled with an inability to produce enough insulin to control blood glucose, and thiazolidinediones (TZDs) are the only current antidiabetic agents that function primarily by increasing insulin sensitivity. However, despite clear benefits in glycemic control, this class of drugs has recently fallen into disuse due to concerns over side effects and adverse events. Here we review the clinical data and attempt to balance the benefits and risks of TZD therapy. We also examine potential mechanisms of action for the beneficial and harmful effects of TZDs, mainly via agonism of the nuclear receptor PPARγ. Based on critical appraisal of both preclinical and clinical studies, we discuss the prospect of harnessing the insulin sensitizing effects of PPARγ for more effective, safe, and potentially personalized treatments of type 2 diabetes.
MeSH term(s)	Animals ; Cardiovascular Diseases/drug therapy ; Diabetes Mellitus, Type 2/drug therapy ; Edema/etiology ; Fractures, Bone/drug therapy ; Humans ; Hypoglycemic Agents/adverse effects ; Hypoglycemic Agents/therapeutic use ; Insulin/metabolism ; Non-alcoholic Fatty Liver Disease/drug therapy ; PPAR gamma/agonists ; PPAR gamma/metabolism ; Thiazolidinediones/adverse effects ; Thiazolidinediones/therapeutic use ; Urinary Bladder Neoplasms/drug therapy
Chemical Substances	Hypoglycemic Agents ; Insulin ; PPAR gamma ; Thiazolidinediones
Language	English
Publishing date	2014-09-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2014.08.005
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Zs.A 6169: Show issues

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Article ; Online: Phosphorylated MED1 links transcription recycling and cancer growth.

Nucleic acids research

2022 Volume 50, Issue 8, Page(s) 4450–4463

Abstract: Mediator activates RNA polymerase II (Pol II) function during transcription, but it remains unclear whether Mediator is able to travel with Pol II and regulate Pol II transcription beyond the initiation and early elongation steps. By using in vitro and ... ...

Abstract	Mediator activates RNA polymerase II (Pol II) function during transcription, but it remains unclear whether Mediator is able to travel with Pol II and regulate Pol II transcription beyond the initiation and early elongation steps. By using in vitro and in vivo transcription recycling assays, we find that human Mediator 1 (MED1), when phosphorylated at the mammal-specific threonine 1032 by cyclin-dependent kinase 9 (CDK9), dynamically moves along with Pol II throughout the transcribed genes to drive Pol II recycling after the initial round of transcription. Mechanistically, MED31 mediates the recycling of phosphorylated MED1 and Pol II, enhancing mRNA output during the transcription recycling process. Importantly, MED1 phosphorylation increases during prostate cancer progression to the lethal phase, and pharmacological inhibition of CDK9 decreases prostate tumor growth by decreasing MED1 phosphorylation and Pol II recycling. Our results reveal a novel role of MED1 in Pol II transcription and identify phosphorylated MED1 as a targetable driver of dysregulated Pol II recycling in cancer.
MeSH term(s)	Animals ; Humans ; Male ; Mammals/genetics ; Mediator Complex/metabolism ; Mediator Complex Subunit 1/genetics ; Neoplasms/genetics ; Phosphorylation ; RNA Polymerase II/metabolism ; Transcription, Genetic
Chemical Substances	MED1 protein, human ; MED31 protein, human ; Mediator Complex ; Mediator Complex Subunit 1 ; RNA Polymerase II (EC 2.7.7.-)
Language	English
Publishing date	2022-04-29
Publishing country	England
Document type	Journal Article
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkac246
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Zs.A 1067: Show issues

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Article ; Online: Shared PPARα/γ Target Genes Regulate Brown Adipocyte Thermogenic Function.

Shen, Yachen / Su, Yvonne / Silva, Francisco J / Weller, Angela H / Sostre-Colón, Jaimarie / Titchenell, Paul M / Steger, David J / Seale, Patrick / Soccio, Raymond E

Cell reports

2020 Volume 30, Issue 9, Page(s) 3079–3091.e5

Abstract: Brown adipose tissue (BAT) generates heat to maintain body temperature and suppress obesity. Agonists for nuclear receptors PPARα and PPARγ both affect brown adipocyte function, yet the interplay between these factors in BAT is uncertain. Here, we report ...

Abstract	Brown adipose tissue (BAT) generates heat to maintain body temperature and suppress obesity. Agonists for nuclear receptors PPARα and PPARγ both affect brown adipocyte function, yet the interplay between these factors in BAT is uncertain. Here, we report that PPARα shares most genomic binding sites with PPARγ, and these common binding sites are more related to BAT function than PPARγ-selective sites without PPARα. Integrating PPARα and PPARγ genomic occupancy with cold-responsive BAT transcriptomes identifies a subset of 16 genes with potential relevance to BAT function. Among these, we focused on the lysosomal protease cathepsin Z (CTSZ) and showed it is necessary for mitochondrial respiration in both mouse and human brown adipocytes. Thus, CTSZ is a shared PPARα/γ target gene in BAT and a regulator of brown adipocyte thermogenic function.
MeSH term(s)	Adipocytes, Brown/metabolism ; Adipose Tissue, Brown/metabolism ; Animals ; Base Sequence ; Binding Sites ; Cathepsin Z/genetics ; Cathepsin Z/metabolism ; Cold Temperature ; Genome ; Humans ; Male ; Mice, Inbred C57BL ; PPAR alpha/agonists ; PPAR alpha/metabolism ; PPAR gamma/agonists ; PPAR gamma/metabolism ; Protein Binding ; Thermogenesis/genetics
Chemical Substances	PPAR alpha ; PPAR gamma ; Cathepsin Z (EC 3.4.18.1) ; Ctsz protein, mouse (EC 3.4.18.1)
Language	English
Publishing date	2020-03-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2020.02.032
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: ILRUN

Bi, Xin / Kuwano, Takashi / Lee, Paul C / Millar, John S / Li, Li / Shen, Yachen / Soccio, Raymond E / Hand, Nicholas J / Rader, Daniel J

Circulation research

2020 Volume 127, Issue 11, Page(s) 1347–1361

Abstract: Rationale: Single-nucleotide polymorphisms near the : Objective: To investigate the role of ILRUN in plasma lipid and lipoprotein metabolism.: Methods and results: ILRUN: Conclusions: These findings establish ILRUN as a novel regulator of lipid ...

Abstract	Rationale: Single-nucleotide polymorphisms near the Objective: To investigate the role of ILRUN in plasma lipid and lipoprotein metabolism. Methods and results: ILRUN Conclusions: These findings establish ILRUN as a novel regulator of lipid metabolism that promotes hepatic lipoprotein production. Our results also provide functional evidence that
MeSH term(s)	Animals ; Blood Glucose/metabolism ; COS Cells ; Cell Line, Tumor ; Chlorocebus aethiops ; Cholesterol, HDL/blood ; Cholesterol, HDL/genetics ; Gene Expression Regulation ; Glucose Intolerance/blood ; Glucose Intolerance/genetics ; HEK293 Cells ; Hepatocytes/metabolism ; Humans ; Lipoproteins/blood ; Lipoproteins/genetics ; Lipoproteins, VLDL/blood ; Lipoproteins, VLDL/genetics ; Liver/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; PPAR alpha/genetics ; PPAR alpha/metabolism ; Protein Binding ; Retinoid X Receptor alpha/genetics ; Retinoid X Receptor alpha/metabolism ; Transcriptome ; Triglycerides/blood ; Triglycerides/genetics ; Ubiquitination
Chemical Substances	Blood Glucose ; Cholesterol, HDL ; ILRUN protein, human ; Lipoproteins ; Lipoproteins, VLDL ; Neoplasm Proteins ; PPAR alpha ; Ppara protein, mouse ; Retinoid X Receptor alpha ; Triglycerides ; very low density lipoprotein triglyceride
Language	English
Publishing date	2020-09-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.120.317175
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Ui IV Zs.70: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Ui IV Zs.60: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Natural human genetic variation determines basal and inducible expression of

Benson, Kiara K / Hu, Wenxiang / Weller, Angela H / Bennett, Alexis H / Chen, Eric R / Khetarpal, Sumeet A / Yoshino, Satoshi / Bone, William P / Wang, Lin / Rabinowitz, Joshua D / Voight, Benjamin F / Soccio, Raymond E

Proceedings of the National Academy of Sciences of the United States of America

2019 Volume 116, Issue 46, Page(s) 23232–23242

Abstract: PM20D1 is a candidate thermogenic enzyme in mouse fat, with its expression cold-induced and enriched in brown versus white adipocytes. Thiazolidinedione (TZD) antidiabetic drugs, which activate the peroxisome proliferator-activated receptor-γ (PPARγ) ... ...

Abstract	PM20D1 is a candidate thermogenic enzyme in mouse fat, with its expression cold-induced and enriched in brown versus white adipocytes. Thiazolidinedione (TZD) antidiabetic drugs, which activate the peroxisome proliferator-activated receptor-γ (PPARγ) nuclear receptor, are potent stimuli for adipocyte browning yet fail to induce
MeSH term(s)	Adipocytes/metabolism ; Adipose Tissue/metabolism ; Amidohydrolases/genetics ; Amidohydrolases/metabolism ; Animals ; Gene Expression ; Gene Expression Regulation ; Genetic Variation ; Humans ; Male ; Mice ; Obesity/genetics ; PPAR gamma/metabolism ; Phenotype ; Thiazolidinediones
Chemical Substances	PPAR gamma ; Thiazolidinediones ; 2,4-thiazolidinedione (AA68LXK93C) ; Amidohydrolases (EC 3.5.-) ; PM20D1 protein, human (EC 3.5.-)
Language	English
Publishing date	2019-10-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1913199116
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Zs.A 1148: Show issues

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Article ; Online: Shared PPARα/γ Target Genes Regulate Brown Adipocyte Thermogenic Function

Yachen Shen / Yvonne Su / Francisco J. Silva / Angela H. Weller / Jaimarie Sostre-Colón / Paul M. Titchenell / David J. Steger / Patrick Seale / Raymond E. Soccio

Cell Reports, Vol 30, Iss 9, Pp 3079-3091.e

2020 Volume 5

Abstract: Summary: Brown adipose tissue (BAT) generates heat to maintain body temperature and suppress obesity. Agonists for nuclear receptors PPARα and PPARγ both affect brown adipocyte function, yet the interplay between these factors in BAT is uncertain. Here, ... ...

Abstract	Summary: Brown adipose tissue (BAT) generates heat to maintain body temperature and suppress obesity. Agonists for nuclear receptors PPARα and PPARγ both affect brown adipocyte function, yet the interplay between these factors in BAT is uncertain. Here, we report that PPARα shares most genomic binding sites with PPARγ, and these common binding sites are more related to BAT function than PPARγ-selective sites without PPARα. Integrating PPARα and PPARγ genomic occupancy with cold-responsive BAT transcriptomes identifies a subset of 16 genes with potential relevance to BAT function. Among these, we focused on the lysosomal protease cathepsin Z (CTSZ) and showed it is necessary for mitochondrial respiration in both mouse and human brown adipocytes. Thus, CTSZ is a shared PPARα/γ target gene in BAT and a regulator of brown adipocyte thermogenic function. : Brown adipocytes uniquely express high levels of PPARα and PPARγ, yet the interplay between these two nuclear receptors was unknown. Shen et al. show PPARα co-occupies regulatory DNA with PPARγ. Shared target genes of both, including the candidate CTSZ, reveal brown fat function better than PPARγ targets alone. Keywords: brown adipocytes, PPARα, PPARγ, rosiglitazone, fenofibrate, CTSZ, thermogenesis
Keywords	Biology (General) ; QH301-705.5
Language	English
Publishing date	2020-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Patient Adipose Stem Cell-Derived Adipocytes Reveal Genetic Variation that Predicts Antidiabetic Drug Response.

Hu, Wenxiang / Jiang, Chunjie / Guan, Dongyin / Dierickx, Pieterjan / Zhang, Rong / Moscati, Arden / Nadkarni, Girish N / Steger, David J / Loos, Ruth J F / Hu, Cheng / Jia, Weiping / Soccio, Raymond E / Lazar, Mitchell A

Cell stem cell

2019 Volume 24, Issue 2, Page(s) 299–308.e6

Abstract: Thiazolidinedione drugs (TZDs) target the transcriptional activity of peroxisome proliferator activated receptor γ (PPARγ) to reverse insulin resistance in type 2 diabetes, but side effects limit their clinical use. Here, using human adipose stem cell- ... ...

Abstract	Thiazolidinedione drugs (TZDs) target the transcriptional activity of peroxisome proliferator activated receptor γ (PPARγ) to reverse insulin resistance in type 2 diabetes, but side effects limit their clinical use. Here, using human adipose stem cell-derived adipocytes, we demonstrate that SNPs were enriched at sites of patient-specific PPARγ binding, which correlated with the individual-specific effects of the TZD rosiglitazone (rosi) on gene expression. Rosi induction of ABCA1, which regulates cholesterol metabolism, was dependent upon SNP rs4743771, which modulated PPARγ binding by influencing the genomic occupancy of its cooperating factor, NFIA. Conversion of rs4743771 from the inactive SNP allele to the active one by clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9-mediated editing rescued PPARγ binding and rosi induction of ABCA1 expression. Moreover, rs4743771 is a major determinant of undesired serum cholesterol increases in rosi-treated diabetics. These data highlight human genetic variation that impacts PPARγ genomic occupancy and patient responses to antidiabetic drugs, with implications for developing personalized therapies for metabolic disorders.
MeSH term(s)	ATP Binding Cassette Transporter 1/genetics ; ATP Binding Cassette Transporter 1/metabolism ; Adipocytes/cytology ; Adipocytes/drug effects ; Adipocytes/metabolism ; Adipose Tissue/cytology ; Adult ; Aged ; Base Sequence ; Cell Line ; Cholesterol/metabolism ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/genetics ; Gene Editing ; Genetic Loci ; Genetic Variation ; Humans ; Hypoglycemic Agents/pharmacology ; Hypoglycemic Agents/therapeutic use ; Middle Aged ; NFI Transcription Factors/metabolism ; PPAR gamma/metabolism ; Polymorphism, Single Nucleotide/genetics ; Protein Binding/drug effects ; Rosiglitazone/pharmacology ; Stem Cells/cytology ; Stem Cells/drug effects ; Stem Cells/metabolism
Chemical Substances	ABCA1 protein, human ; ATP Binding Cassette Transporter 1 ; Hypoglycemic Agents ; NFI Transcription Factors ; NFIA protein, human ; PPAR gamma ; Rosiglitazone (05V02F2KDG) ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2019-01-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2018.11.018
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Zs.A 6589: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 75: Show issues

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Article: StAR-related lipid transfer (START) proteins: mediators of intracellular lipid metabolism.

Soccio, Raymond E / Breslow, Jan L

The Journal of biological chemistry

2003 Volume 278, Issue 25, Page(s) 22183–22186

MeSH term(s)	Animals ; Carrier Proteins/chemistry ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cholesterol/metabolism ; Evolution, Molecular ; Humans ; Intracellular Membranes/physiology ; Kinetics ; Lipid Metabolism ; Mitochondria/physiology ; Neoplasm Proteins/chemistry ; Neoplasm Proteins/metabolism ; Signal Transduction
Chemical Substances	Carrier Proteins ; Neoplasm Proteins ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2003-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.R300003200
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