HCSGD entry for ACAN


1. General information

Official gene symbolACAN
Entrez ID176
Gene full nameaggrecan
Other gene symbolsAGC1 AGCAN CSPG1 CSPGCP MSK16 SEDK
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0001501Skeletal system developmentNASbiological_process
GO:0001502Cartilage condensationIEAbiological_process
GO:0002063Chondrocyte developmentIEAbiological_process
GO:0005201Extracellular matrix structural constituentTASmolecular_function
GO:0005509Calcium ion bindingIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005540Hyaluronic acid bindingIEAmolecular_function
GO:0005576Extracellular regionTAScellular_component
GO:0005578Proteinaceous extracellular matrixIEAcellular_component
GO:0005604Basement membraneIEAcellular_component
GO:0005796Golgi lumenTAScellular_component
GO:0005975Carbohydrate metabolic processTASbiological_process
GO:0006508ProteolysisNASbiological_process
GO:0007155Cell adhesionIEAbiological_process
GO:0018146Keratan sulfate biosynthetic processTASbiological_process
GO:0030166Proteoglycan biosynthetic processIEAbiological_process
GO:0030198Extracellular matrix organizationTASbiological_process
GO:0030199Collagen fibril organizationIEAbiological_process
GO:0030203Glycosaminoglycan metabolic processTASbiological_process
GO:0030246Carbohydrate bindingIEAmolecular_function
GO:0031012Extracellular matrixIDAcellular_component
GO:0042339Keratan sulfate metabolic processTASbiological_process
GO:0042340Keratan sulfate catabolic processTASbiological_process
GO:0043202Lysosomal lumenTAScellular_component
GO:0044281Small molecule metabolic processTASbiological_process
GO:0046872Metal ion bindingIEAmolecular_function
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.21812713040.20927394860.89834520420.8846273486

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Down-0.0012219650
GSE13712_SHEARUp0.0007864076
GSE13712_STATICUp0.0440868452
GSE19018Up0.0457967273
GSE19899_A1Down-0.1202796145
GSE19899_A2Down-0.0902952990
PubMed_21979375_A1Down-1.0512320498
PubMed_21979375_A2Down-0.2338880748
GSE35957Up0.1793453420
GSE36640Down-0.0911297859
GSE54402Up0.1633963071
GSE9593Down-0.0447546362
GSE43922Up0.0281856951
GSE24585Down-0.0229251945
GSE37065Up0.0299130980
GSE28863_A1Down-0.3698465501
GSE28863_A2Up0.0405473580
GSE28863_A3Up0.9055644525
GSE28863_A4Up0.2197544645
GSE48662Up0.3189449404

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase
No target information from mirTarBase
  • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 15 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

26749742Besides, the aggrecan and collagen type II expression were examined by toluidine blue and immunocytochemistry staining respectively
26337541H2O2-senescent cells were found to possess a catabolic phenotype, mainly characterised by the up-regulation of extracellular matrix-degrading enzymes (MMP-1, -2, -9 and ADAMTS-5) and the down-regulation of their inhibitors (TIMPs), as well as of several proteoglycans, including aggrecan, the major component of the nucleus pulposus
25826898Senescence marker (p16INK4a) and disc degeneration markers [A disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS 5), Aggrecan, and Sry-related HMG box transcription factor 9 (Sox-9)] were determined in the NP specimens with immunohistochemistry and Western blot
25826898The protein expressions of Aggrecan and Sox-9 in the NP with grade IV degeneration were significantly lower than those in the NP with grade III degeneration (P < 0
25087910Glucosamine attenuated the decrease of aggrecan and prevented the apoptosis of the NP cells induced by IL-1beta, whereas 3-MA partly reversed these effects
23879090After corresponding treatment, Western blot was used for determining the protein expressions of SIRT1, Aggrecan, and collagen type II; real-time fluorescence quantitative PCR was used for detecting SIRT1 mRNA expression
23879090The protein expressions of SIRT1, collagen type II, and Aggrecan in group B were significantly improved when compared with that in group A (P < 0
23438440Whole bovine discs were cultured to examine cellular (anabolic/catabolic gene expression, cell viability and senescence using beta-galactosidase) and structural (histology and aggrecan degradation) changes in response to TNFalpha treatment
23438440Data indicates that TNFalpha increased aggrecan degradation products and suggests increased beta-galactosidase staining at 21 days without any recovery
23262094Expression of the protease ADAMTS4 and aggrecan proteolytic fragments was significantly increased
23238821The proteoglycan and collagen II in the extracellular matrix and the aggrecan and collagen II mRNA expression in NP cells of diabetic rats were decreased compared with the control group
22531458Total disc proteoglycan (PG) content [1,9-dimethylmethylene blue (DMMB) assay], aggrecan proteolysis (immunobloting analysis), and cellular senescence (p16INK4a immunohistochemistry) were analyzed
22531458Exposure to tobacco smoke dramatically increased metalloproteinase-mediated proteolysis of disc aggrecan within its interglobular domain (IGD)
22531458Cleavage of aggrecan IGD is extremely detrimental as this results in the loss of the entire glycosaminoglycan-attachment region of aggrecan, which is vital for attracting water necessary to counteract compressive forces
22454193The expression levels of mRNAs encoding aggrecan (ACAN), a major structural proteoglycan, type II collagen (COL2A1), and metalloproteinases (MMP) -1, -3, and -13, respectively, were determined using real-time PCR
22454193RESULTS: Chondrocytes stimulated by IL-1beta showed increased MMP-1, MMP-3, and MMP-13 levels, whereas the expression of COL2A1 and ACAN decreased
22454193However, in cells co-treated with IL-1beta and Rg3, the levels of MMP-1 and MMP-13 were lower than in cells treated with IL-1beta alone, and COL2A1 and ACAN expression levels recovered from the low values seen when cultured only in the presence of IL-1beta
21627568Chondrogenesis, proteoglycan deposition, collagen type II protein expression, collagen type 2A1 (Col2AI), and aggrecan (Acan) mRNA expression were less in pellets formed with later passages of TDSCs after chondrogenic induction
20533544OBJECTIVE: To determine whether intervertebral disc (IVD) cells express beta-catenin and to assess the role of the WNT/beta-catenin signaling pathway in cellular senescence and aggrecan synthesis
20533544Activation of WNT/beta-catenin signaling also regulated the expression of aggrecan
19058142After 7 days, DNA and sulfated glycosaminoglycan contents were analyzed along with real time, quantitative reverse transcription-polymerase chain reaction analysis for collagen types I and II, aggrecan, and matrix metalloproteinase-3 gene expression
18024225Gene expression of types I, II, and VI collagen, aggrecan, and chondroitin-6-sulfotransferase in the human annulus: in situ hybridization findings
18024225PURPOSE: To determine the percentage and patterns of gene expression for types I, II, and VI collagen, aggrecan, and chondroitin-6-sulfotransferase in the human annulus
18024225OUTCOME MEASURES: The percentages of cells in the human annulus expressing type I, II, and VI collagen, aggrecan, and chondroitin-6-sulfotransferase
18024225METHODS: In situ hybridization, a technique with high temporal and spatial resolution, was used to detect gene expression of types I, II, and VI collagen, aggrecan, and chondroitin-6 sulfotransferase in cells in adjacent sections of annulus from discs with Thompson grades of II, III, and IV
180242258% of cells expressed aggrecan, 38
12721352As chondrocytes age, they synthesize smaller, less uniform aggrecan molecules and less functional link proteins, their mitotic and synthetic activity decline, and their responsiveness to anabolic mechanical stimuli and growth factors decreases
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