Adiponectin (ADIPOQ)
The protein contains 244 amino acids for an estimated molecular weight of 26414 Da.
Important adipokine involved in the control of fat metabolism and insulin sensitivity, with direct anti-diabetic, anti-atherogenic and anti-inflammatory activities. Stimulates AMPK phosphorylation and activation in the liver and the skeletal muscle, enhancing glucose utilization and fatty-acid combustion. Antagonizes TNF-alpha by negatively regulating its expression in various tissues such as liver and macrophages, and also by counteracting its effects. Inhibits endothelial NF-kappa-B signaling through a cAMP-dependent pathway. May play a role in cell growth, angiogenesis and tissue remodeling by binding and sequestering various growth factors with distinct binding affinities, depending on the type of complex, LMW, MMW or HMW. (updated: Oct. 10, 2018)
Protein identification was indicated in the following studies:
Methods
The following articles were analysed to gather the proteome content of erythrocytes.
The gene or protein list provided in the studies were processed using the ID mapping API of Uniprot in September 2018. The number of proteins identified and mapped without ambiguity in these studies is indicated below.
Only Swiss-Prot entries (reviewed) were considered for protein evidence assignation.
| Publication | Identification 1 | Uniprot mapping 2 | Not mapped / Obsolete | TrEMBL | Swiss-Prot |
|---|---|---|---|---|---|
| Goodman (2013) | 2289 (gene list) | 2278 | 53 | 20599 | 2269 |
| Lange (2014) | 1234 | 1234 | 7 | 28 | 1224 |
| Hegedus (2015) | 2638 | 2622 | 0 | 235 | 2387 |
| Wilson (2016) | 1658 | 1528 | 170 | 291 | 1068 |
| d'Alessandro (2017) | 1826 | 1817 | 2 | 0 | 1815 |
| Bryk (2017) | 2090 | 2060 | 10 | 108 | 1942 |
| Chu (2018) | 1853 | 1804 | 55 | 362 | 1387 |
1 as available in the article and/or in supplementary material
2 uniprot mapping returns all protein isoforms as one entry
The compilation of older studies can be retrieved from the Red Blood Cell Collection database.
The data and differentiation stages presented below come from the proteomic study and analysis performed by our partners of the GReX consortium, more details are available in their published work.
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No binding partner found
Biological Process
Brown fat cell differentiation
Cellular response to cAMP
Cellular response to drug
Cellular response to epinephrine stimulus
Cellular response to insulin stimulus
Circadian rhythm
Detection of oxidative stress
Fatty acid beta-oxidation
Fatty acid oxidation
Generation of precursor metabolites and energy
Glucose homeostasis
Glucose metabolic process
Low-density lipoprotein particle clearance
Negative regulation of blood pressure
Negative regulation of cell migration
Negative regulation of cold-induced thermogenesis
Negative regulation of DNA biosynthetic process
Negative regulation of ERK1 and ERK2 cascade
Negative regulation of fat cell differentiation
Negative regulation of gluconeogenesis
Negative regulation of granulocyte differentiation
Negative regulation of heterotypic cell-cell adhesion
Negative regulation of hormone secretion
Negative regulation of I-kappaB kinase/NF-kappaB signaling
Negative regulation of inflammatory response
Negative regulation of intracellular protein transport
Negative regulation of low-density lipoprotein particle receptor biosynthetic process
Negative regulation of macrophage derived foam cell differentiation
Negative regulation of macrophage differentiation
Negative regulation of MAP kinase activity
Negative regulation of metanephric mesenchymal cell migration
Negative regulation of phagocytosis
Negative regulation of platelet-derived growth factor receptor signaling pathway
Negative regulation of platelet-derived growth factor receptor-alpha signaling pathway
Negative regulation of protein autophosphorylation
Negative regulation of receptor binding
Negative regulation of synaptic transmission
Negative regulation of transcription, DNA-templated
Negative regulation of tumor necrosis factor production
Negative regulation of tumor necrosis factor-mediated signaling pathway
Negative regulation of vascular associated smooth muscle cell migration
Negative regulation of vascular associated smooth muscle cell proliferation
Positive regulation of cAMP-dependent protein kinase activity
Positive regulation of cellular protein metabolic process
Positive regulation of cholesterol efflux
Positive regulation of cold-induced thermogenesis
Positive regulation of fatty acid metabolic process
Positive regulation of glucose import
Positive regulation of glycogen (starch) synthase activity
Positive regulation of I-kappaB kinase/NF-kappaB signaling
Positive regulation of interleukin-8 production
Positive regulation of metanephric glomerular visceral epithelial cell development
Positive regulation of monocyte chemotactic protein-1 production
Positive regulation of myeloid cell apoptotic process
Positive regulation of peptidyl-tyrosine phosphorylation
Positive regulation of protein kinase A signaling
Positive regulation of protein phosphorylation
Positive regulation of renal albumin absorption
Positive regulation of signal transduction
Protein heterotrimerization
Protein homooligomerization
Protein localization to plasma membrane
Regulation of fatty acid biosynthetic process
Regulation of glucose metabolic process
Response to activity
Response to bacterium
Response to ethanol
Response to glucocorticoid
Response to glucose
Response to hypoxia
Response to linoleic acid
Response to nutrient
Response to sucrose
Response to tumor necrosis factor
The reference OMIM entry for this protein is 125853
Diabetes mellitus, noninsulin-dependent; niddm
Diabetes mellitus, type ii; t2d
Noninsulin-dependent diabetes mellitus
Maturity-onset diabetes insulin resistance, susceptibility to, included
Diabetes mellitus, type 2, protection against, inclu
A number sign (#) is used with this entry because of evidence that more than one gene is involved in the causation of noninsulin-dependent diabetes mellitus (NIDDM). See 601283 for description of a form of NIDDM linked to 2q, which may be caused by mutation in the gene encoding calpain-10 (CAPN10; 605286). See 601407 for description of a chromosome 12q locus, NIDDM2, found in a Finnish population. See 603694 for description of a locus on chromosome 20, NIDDM3. See 608036 for description of a locus on chromosome 5q34-q35, NIDDM4. See 616087 for description of NIDDM5, which comprises susceptibility related to a nonsense mutation in the TBC1D4 gene (612465) on chromosome 13q22. A mutation has been observed in hepatocyte nuclear factor-4-alpha (HNF4A; 600281.0004) in a French family with NIDDM of late onset. Mutations in the NEUROD1 gene (601724) on chromosome 2q32 were found to cause type II diabetes mellitus in 2 families. Mutation in the GLUT2 glucose transporter was associated with NIDDM in 1 patient (138160.0001). Mutation in the MAPK8IP1 gene, which encodes the islet-brain-1 protein, was found in a family with type II diabetes in individuals in 4 successive generations (604641.0001). Polymorphism in the KCNJ11 gene (600937.0014) confers susceptibility. In French white families, Vionnet et al. (2000) found evidence for a susceptibility locus for type II diabetes on 3q27-qter. They confirmed the diabetes susceptibility locus on 1q21-q24 reported by Elbein et al. (1999) in whites and by Hanson et al. (1998) in Pima Indians. A mutation in the GPD2 gene (138430.0001) on chromosome 2q24.1, encoding mitochondrial glycerophosphate dehydrogenase, was found in a patient with type II diabetes mellitus and in his glucose-intolerant half sister. Mutations in the PAX4 gene (167413) have been identified in patients with type II diabetes. Triggs-Raine et al. (2002) stated that in the Oji-Cree, a gly319-to-ser change in HNF1-alpha (142410.0008) behaves as a susceptibility allele for type II diabetes. Mutation in the HNF1B gene (189907.0007) was found in 2 Japanese patients with typical late-onset type II diabetes. Mutations in the IRS1 gene (147545) have been found in patients with type II diabetes. A missense mutation in the AKT2 gene (164731.0001) caused autosomal dominant type II diabetes in 1 family. A (single-nucleotide polymorphism) SNP in the 3-prime untranslated region of the resistin gene (605565.0001) was associated with susceptibility to diabetes and to insulin resistance-related hypertension in Chinese subjects. Susceptibility to insulin resistance has been associated with polymorphism in the TCF1 (142410.0011), PPP1R3A (600917.0001), PTPN1 (176885.0001), ENPP1 (173335.0006), IRS1 (147545.0002), and EPHX2 (132811.0001) genes. The K121Q polymorphism of ENPP1 (173335.0006) is associated with susceptibility to type II diabetes; a haplotype defined by 3 SNPs of this gene, including K121Q, is associated with obesity, glucose intolerance, and type II diabetes. A SNP in the promoter region of the hepatic lipase gene (151670.0004) predicts conversion from impaired glucose tolerance to type II diabetes. Variants of transcription factor 7-like-2 (TCF7L2; 602228.0001), located on 10q, have also been found to confer risk of type II diabetes. A common sequence variant, dbSNP rs10811661, on chromosome 9p21 near the CDKN2A (600160) and CDKN2B (600431) genes has been associated with risk of type II diabetes. Variation in the PPARG gene (601487) has been a ... More on the omim web site
Nov. 16, 2018: Protein entry updated
Automatic update: OMIM entry 125853 was added.
Oct. 19, 2018: Additional information
Initial protein addition to the database. This entry was referenced in Bryk and co-workers. (2017).