Cited by 371Adipokines, Inflammation, and Metabolic DiseasesPeroxisome Proliferator-Activated ReceptorsAdipose Tissue and Metabolism

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Molecular, biochemical and functional characterizations of C1q/TNF family members: adipose-tissue-selective expression patterns, regulation by PPAR-γ agonist, cysteine-mediated oligomerizations, combinatorial associations and metabolic functions

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Wong, G. William, Krawczyk, Sarah A., Kitidis-Mitrokostas, Claire, Revett, Tracy, Gimeno, Ruth, Lodish, Harvey F.·2008·Biochemical Journal

DOI 10.1042/bj20081240PMC PMC3936483

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Abstract

The insulin-sensitizing hormone, adiponectin, belongs to the expanding C1q/TNF (tumour necrosis factor) family of proteins. We recently identified a family of adiponectin paralogues designated as CTRP (C1q/TNF-related protein) 1-7, and in the present study describe CTRP10. In the present study, we show that CTRP1, CTRP2, CTRP3, CTRP5 and CTRP7 transcripts are expressed predominantly by adipose tissue. In contrast, placenta and eye expressed the highest levels of CTRP6 and CTRP10 transcripts respectively. Expression levels of CTRP1, CTRP2, CTRP3, CTRP6 and CTRP7 transcripts are up-regulated in 8-week-old obese (ob/ob) mice relative to lean controls. Treatment of mice with a PPAR-gamma (peroxisome-proliferator-activated receptor-gamma) agonist, rosiglitazone, increased the expression of CTRP1 and decreased CTRP6 transcript levels. All CTRPs are secreted glycoproteins when expressed in mammalian cells. CTRP1, CTRP2, CTRP3, CTRP5 and CTRP6 circulate in the blood and are potential endocrine hormones; their serum levels vary according to the sex and genetic background of mice. Importantly, serum levels of CTRP1 and CTRP6 are increased in adiponectin-null mice. Like adiponectin, all secreted CTRP proteins form trimers as their basic structural units. CTRP3, CTRP5, CTRP6 and CTRP10 trimers are further assembled into higher-order oligomeric complexes via disulfide bonding mediated by their N-terminal cysteine residues. Besides forming homo-oligomers, CTRP1/CTRP6, CTRP2/CTRP7 and adiponectin/CTRP2 are secreted as heterotrimers, thus providing a mechanism to potentially generate functionally distinct ligands. Functional characterization of one such family member, CTRP1, showed that it specifically activates Akt and p44/42-MAPK (mitogen-activated protein kinase) signalling pathways in differentiated mouse myotubes. Moreover, injection of recombinant CTRP1 into mice significantly reduced their serum glucose levels. Thus at least CTRP1 may be considered a novel adipokine. In summary, these molecular, biochemical and functional data provide an important framework to further address the physiological functions and mechanisms of the action of this family of secreted glycoproteins in normal and disease states.

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Retracted
Adipokine C1q/Tumor Necrosis Factor- Related Protein 3 (CTRP3) Attenuates Intestinal Inflammation Via Sirtuin 1/NF-κB Signaling
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CTRP13 ablation improves systemic glucose and lipid metabolism
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Authors: Wong, G. W., Krawczyk, S. A., Kitidis-Mitrokostas, C., Revett, T., Gimeno, R., & Lodish, H. F.
Affiliations: Whitehead Institute for Biomedical Research (US)
Whitehead Institute for Biomedical Research, Cambridge, MA 02142, U.S.A.
Wyeth (US)
Corresponding author: Wong, G. William
Lodish, Harvey F.
ORCID: Wong, G. William
Lodish, Harvey F.
Venue: Biochemical Journal
Publisher: Portland Press Ltd.
Published: 2008-11-12
Volume: 416
Issue: 2
Pages: 161-177
ISSN: 0264-6021 (ISSN-L)
1470-8728
DOI: 10.1042/bj20081240
PMC: PMC3936483
OpenAlex: W2054584654
Cited by: 371
References: 53
Citations by year: 2026: 7 · 2025: 13 · 2024: 20 · 2023: 21 · 2022: 29 · 2021: 30 · 2020: 35 · 2019: 32 · 2018: 26 · 2017: 24 · 2016: 35 · 2015: 27 · 2014: 18 · 2013: 13 · 2012: 18
FWCI: 5.71
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Biochemical Journal (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (1f32dk067835-01)
National Heart, Lung, and Blood Institute (K08HL077499, HL077499-01)
National Institute of Diabetes and Digestive and Kidney Diseases (F32DK067835, R37 DK47618‐19, R37DK047618, R01DK047618)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Keywords: CTRP, adiponectin, adipose tissue, tissue-specific gene expression, PPARγ agonists, rosiglitazone, obesity, heterotrimers, oligomerization, disulfide bonds, Akt signaling, MAPK signaling, myotubes, insulin sensitivity, adipokines
MeSH terms: Adipose Tissue, Animals, Cloning, Molecular, Collagen, Humans, Insulin Resistance, Mice, Inbred Strains, Mice, Transgenic, Proteins, Transfection, Mutagenesis, Site-Directed, Stromal Cells, Plasminogen Activator Inhibitor 1, Adipocytes, Chemokine CCL2, Leptin, PPAR gamma, Mice, Adiponectin

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Molecular, biochemical and functional characterizations of C1q/TNF family members: adipose-tissue-selective expression patterns, regulation by PPAR-γ agonist, cysteine-mediated oligomerizations, combinatorial associations and metabolic functions

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