产品: Aggrecan 抗体
货号: DF7561
描述: Rabbit polyclonal antibody to Aggrecan
应用: WB IHC IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Bovine, Sheep, Rabbit, Dog
分子量: 70,150,250 kDa; 261kD(Calculated).
蛋白号: P16112
RRID: AB_2841055

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产品描述

来源:
Rabbit
应用:
WB 1:1000-3000, IF/ICC 1:100-1:500, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human,Mouse,Rat
预测:
Pig(100%), Bovine(100%), Sheep(100%), Rabbit(100%), Dog(100%)
克隆:
Polyclonal
特异性:
Aggrecan Antibody detects endogenous levels of total Aggrecan.
RRID:
AB_2841055
引用格式: Affinity Biosciences Cat# DF7561, RRID:AB_2841055.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

ACAN; AGC 1; AGC1; AGCAN; Aggrecan 1 (chondroitin sulfate proteoglycan 1, large aggregating proteoglycan, antigen identified by monoclonal antibody A0122); Aggrecan 1; Aggrecan core protein; Aggrecan proteoglycan; Aggrecan structural proteoglycan of cartilage; Aggrecan1; ATEGQV; Cartilage specific proteoglycan core protein; Chondroitin sulfate proteoglycan 1; Chondroitin sulfate proteoglycan 1 large aggregating proteoglycan antigen identified by monoclonal antibody A0122; Chondroitin sulfate proteoglycan core protein 1; CSPG 1; CSPG1; CSPGCP; JSCATE; Large aggregating proteoglycan; mcspg; mgsk16; MSK 16; MSK16; SEDK;

抗原和靶标

免疫原:
Uniprot:
基因/基因ID:
表达:
P16112 PGCA_HUMAN:

Restricted to cartilages.

序列:
MTTLLWVFVTLRVITAAVTVETSDHDNSLSVSIPQPSPLRVLLGTSLTIPCYFIDPMHPVTTAPSTAPLAPRIKWSRVSKEKEVVLLVATEGRVRVNSAYQDKVSLPNYPAIPSDATLEVQSLRSNDSGVYRCEVMHGIEDSEATLEVVVKGIVFHYRAISTRYTLDFDRAQRACLQNSAIIATPEQLQAAYEDGFHQCDAGWLADQTVRYPIHTPREGCYGDKDEFPGVRTYGIRDTNETYDVYCFAEEMEGEVFYATSPEKFTFQEAANECRRLGARLATTGQLYLAWQAGMDMCSAGWLADRSVRYPISKARPNCGGNLLGVRTVYVHANQTGYPDPSSRYDAICYTGEDFVDIPENFFGVGGEEDITVQTVTWPDMELPLPRNITEGEARGSVILTVKPIFEVSPSPLEPEEPFTFAPEIGATAFAEVENETGEATRPWGFPTPGLGPATAFTSEDLVVQVTAVPGQPHLPGGVVFHYRPGPTRYSLTFEEAQQACLRTGAVIASPEQLQAAYEAGYEQCDAGWLRDQTVRYPIVSPRTPCVGDKDSSPGVRTYGVRPSTETYDVYCFVDRLEGEVFFATRLEQFTFQEALEFCESHNATLATTGQLYAAWSRGLDKCYAGWLADGSLRYPIVTPRPACGGDKPGVRTVYLYPNQTGLPDPLSRHHAFCFRGISAVPSPGEEEGGTPTSPSGVEEWIVTQVVPGVAAVPVEEETTAVPSGETTAILEFTTEPENQTEWEPAYTPVGTSPLPGILPTWPPTGAATEESTEGPSATEVPSASEEPSPSEVPFPSEEPSPSEEPFPSVRPFPSVELFPSEEPFPSKEPSPSEEPSASEEPYTPSPPVPSWTELPSSGEESGAPDVSGDFTGSGDVSGHLDFSGQLSGDRASGLPSGDLDSSGLTSTVGSGLPVESGLPSGDEERIEWPSTPTVGELPSGAEILEGSASGVGDLSGLPSGEVLETSASGVGDLSGLPSGEVLETTAPGVEDISGLPSGEVLETTAPGVEDISGLPSGEVLETTAPGVEDISGLPSGEVLETTAPGVEDISGLPSGEVLETTAPGVEDISGLPSGEVLETTAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETAAPGVEDISGLPSGEVLETTAPGVEEISGLPSGEVLETTAPGVDEISGLPSGEVLETTAPGVEEISGLPSGEVLETSTSAVGDLSGLPSGGEVLEISVSGVEDISGLPSGEVVETSASGIEDVSELPSGEGLETSASGVEDLSRLPSGEEVLEISASGFGDLSGLPSGGEGLETSASEVGTDLSGLPSGREGLETSASGAEDLSGLPSGKEDLVGSASGDLDLGKLPSGTLGSGQAPETSGLPSGFSGEYSGVDLGSGPPSGLPDFSGLPSGFPTVSLVDSTLVEVVTASTASELEGRGTIGISGAGEISGLPSSELDISGRASGLPSGTELSGQASGSPDVSGEIPGLFGVSGQPSGFPDTSGETSGVTELSGLSSGQPGISGEASGVLYGTSQPFGITDLSGETSGVPDLSGQPSGLPGFSGATSGVPDLVSGTTSGSGESSGITFVDTSLVEVAPTTFKEEEGLGSVELSGLPSGEADLSGKSGMVDVSGQFSGTVDSSGFTSQTPEFSGLPSGIAEVSGESSRAEIGSSLPSGAYYGSGTPSSFPTVSLVDRTLVESVTQAPTAQEAGEGPSGILELSGAHSGAPDMSGEHSGFLDLSGLQSGLIEPSGEPPGTPYFSGDFASTTNVSGESSVAMGTSGEASGLPEVTLITSEFVEGVTEPTISQELGQRPPVTHTPQLFESSGKVSTAGDISGATPVLPGSGVEVSSVPESSSETSAYPEAGFGASAAPEASREDSGSPDLSETTSAFHEANLERSSGLGVSGSTLTFQEGEASAAPEVSGESTTTSDVGTEAPGLPSATPTASGDRTEISGDLSGHTSQLGVVISTSIPESEWTQQTQRPAETHLEIESSSLLYSGEETHTVETATSPTDASIPASPEWKRESESTAAAPARSCAEEPCGAGTCKETEGHVICLCPPGYTGEHCNIDQEVCEEGWNKYQGHCYRHFPDRETWVDAERRCREQQSHLSSIVTPEEQEFVNNNAQDYQWIGLNDRTIEGDFRWSDGHPMQFENWRPNQPDNFFAAGEDCVVMIWHEKGEWNDVPCNYHLPFTCKKGTVACGEPPVVEHARTFGQKKDRYEINSLVRYQCTEGFVQRHMPTIRCQPSGHWEEPQITCTDPTTYKRRLQKRSSRHPRRSRPSTAH

种属预测

种属预测:

score>80的预测可信度较高,可尝试用于WB检测。*预测模型主要基于免疫原序列比对,结果仅作参考,不作为质保凭据。

Species
Results
Score
Pig
100
Bovine
100
Sheep
100
Dog
100
Rabbit
100
Horse
78
Chicken
67
Xenopus
0
Zebrafish
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

翻译修饰 - P16112 作为底物

Site PTM Type Enzyme
T371 O-Glycosylation
T376 O-Glycosylation
Y536 Phosphorylation
S540 Phosphorylation
N658 N-Glycosylation

研究背景

功能:

This proteoglycan is a major component of extracellular matrix of cartilagenous tissues. A major function of this protein is to resist compression in cartilage. It binds avidly to hyaluronic acid via an N-terminal globular region.

翻译修饰:

Contains mostly chondroitin sulfate, but also keratan sulfate chains, N-linked and O-linked oligosaccharides. The release of aggrecan fragments from articular cartilage into the synovial fluid at all stages of human osteoarthritis is the result of cleavage by aggrecanase.

细胞定位:

Secreted>Extracellular space>Extracellular matrix.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
组织特异性:

Restricted to cartilages.

亚基结构:

Interacts with FBLN1 (By similarity). Interacts with COMP.

蛋白家族:

Two globular domains, G1 and G2, comprise the N-terminus of the proteoglycan, while another globular region, G3, makes up the C-terminus. G1 contains Link domains and thus consists of three disulfide-bonded loop structures designated as the A, B, B' motifs. G2 is similar to G1. The keratan sulfate (KS) and the chondroitin sulfate (CS) attachment domains lie between G2 and G3.

Belongs to the aggrecan/versican proteoglycan family.

文献引用

1). Hydrogen Ion Capturing Hydrogel Microspheres for Reversing Inflammaging. Advanced materials (Deerfield Beach, Fla.), 2024 (PubMed: 37699155) [IF=29.4]

2). An anti-inflammatory and neuroprotective biomimetic nanoplatform for repairing spinal cord injury. Bioactive Materials, 2022 (PubMed: 35845318) [IF=18.9]

3). Loss of DDRGK1 impairs IRE1α UFMylation in spondyloepiphyseal dysplasia. International Journal of Biological Sciences, 2023 (PubMed: 37781516) [IF=9.2]

Application: IF/ICC    Species: Mouse    Sample:

Figure 6 Loss of DDRGK1 or the K268R mutation led to IRE1α degradation and ER stress aggravation in the growth plate cells of mice in vivo. (A) Immunofluorescence analysis of SOX9, Aggrecan, IRE1α and CHOP expression in the lower limbs of the WT and cKO mice shown in Figure ​Figure1A;1A; the growth plate is the focus. (B) Quantification of the integrated optical density (IOD)/DAPI stain intensity levels of SOX9, Aggrecan, IRE1α and CHOP in the images shown in panel (A). (C) Alcian blue staining of primary chondrocytes from WT and mutant mice 9 days after high-density culturing in chondrogenesis medium. (D) Quantification of the relative IOD/area ratio in the Alcian blue-stained cells shown in panel (C). (E) Safranin O-Fast Green staining of the lower limbs in WT and mutant mice; the growth plate is the focus. (F) Quantification of the length of the hypertrophy zone (HZ) shown in panel (E). (G) TUNEL immunofluorescence staining of the lower limbs of the WT and cKO mice shown in Figure ​Figure1A1A with focus on the growth plate. (H) Quantification of the percentage of TUNEL-positive cells in the growth plate shown in panel (G). (I) Reverse transcription-quantitative PCR analysis performed to determine the relative mRNA expression levels of ATF4, BIP and CHOP in primary WT and Mutant mouse chondrocytes treated with or without thapsigargin (Tg) for 24 h; β-actin was the internal reference. (J) Western blot analysis of DDRGK1, IRE1α, BIP, ATF4 and CHOP of primary WT and mutant mouse chondrocytes treated with or without Tg for 24 h; β-actin was the loading control. (K) Immunofluorescence analysis of IRE1α, XBP-1s and CHOP expression in the lower limbs of the WT and mutant mice shown in panel (E); the growth plate is the focus. (L) Quantification of the IOD/DAPI stain intensity levels of IRE1α, XBP-1s and CHOP in the chondrocytes shown in panel (K). (M) Western blot analysis of cleaved and full-length PARP and cleaved Caspase 3 in primary in WT and mutant mouse chondrocytes treated with or without Tg for 24 h; β-actin was the loading control. All data are presented as the mean ± SD from three or more experiments.

4). TMF inhibits extracellular matrix degradation by regulating the C/EBPβ/ADAMTS5 signaling pathway in osteoarthritis. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2024 (PubMed: 38554527) [IF=7.5]

Application: IHC    Species: Rat    Sample:

Fig. 1. The effect of TMF on the articular cartilage of OA rats (n = 6) was investigated. (A) The articular cartilage was stained with H/E. IHC assays were used to detect the altered expression of Aggrecan (B–C), ADAMTS5 (D–E), and Caspase3 (F–G) in the cartilage.

5). Vitamin K2 ameliorates osteoarthritis by suppressing ferroptosis and extracellular matrix degradation through activation GPX4's dual functions. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2024 (PubMed: 38759289) [IF=7.5]

Application: WB    Species: Rat    Sample:

Fig. 8. GPX4 inhibitor RSL3 substantially attenuates VK2 protection of chondrocytes. (A-I) WB results for GPX4, NFκB, pMAPK/MAPK, Aggrecan, CollagenⅡ, SOX9, MMP3, MMP13 and Tubulin; (J) Quantitive analysis of relative Glutathione Peroxidase Activity; (K-L) GSH contents and ratio of GSH/GSSG; (M) Quantitative results of MDA content assay.

6). Bioprinted biomimetic hydrogel matrices guiding stem cell aggregates for enhanced chondrogenesis and cartilage regeneration. Journal of materials chemistry. B, 2024 (PubMed: 38700242) [IF=7.0]

7). Lysyl oxidase inhibits TNF-α induced rat nucleus pulposus cell apoptosis via regulating Fas/FasL pathway and the p53 pathways. LIFE SCIENCES, 2020 (PubMed: 32979358) [IF=6.1]

Application: WB    Species: rat    Sample: NP cells

Fig. 3. |LOX improved the ECM expression pattern in TNF-α-treated rat NP cells. A. and B. Relative mRNA expressions of type II collagen and aggrecan in rat NP cells with different treatments were analyzed by RT-qPCR. C. Protein expressions of type II collagen and aggrecan in rat NP cells with different treatments were analyzed by western blot.

8). MicroRNA-145 overexpression attenuates apoptosis and increases matrix synthesis in nucleus pulposus cells. LIFE SCIENCES, 2019 (PubMed: 30797016) [IF=6.1]

Application: WB    Species: rat    Sample: NP cells

Fig. 3. |miR-145 increased matrix metabolism in rat NP cells.(A, B) Real-time PCR analysis was performed to evaluate the mRNA expression of aggrecan (A) and collagen IIa (B) after a single transfection with agomir-145 or miR-155 inhibitors. (C, D, E) Western blotting (C) and subsequent densitometric analysis (D) demonstrated that aggrecan (C, E) and collagen IIa (D, E) protein were significantly upregulated in rat NP cells after transfection with agomir-145.

9). L-Glutamine alleviates osteoarthritis by regulating lncRNA-NKILA expression through the TGF-β1/SMAD2/3 signalling pathway. Clinical Science, 2022 (PubMed: 35730575) [IF=6.0]

10). TRIM38 protects chondrocytes from IL-1β-induced apoptosis and degeneration via negatively modulating nuclear factor (NF)-κB signaling. International Immunopharmacology, 2021 (PubMed: 34426118) [IF=5.6]

Application: WB    Species: Mouse    Sample: chondrocytes

Fig. 4. The effects of TRIM38 depletion on IL-1β-induced degeneration of chondrocytes. (A, B) The effects of TRIM38 overexpression on the levels of MMP-3, MMP- 13, ACAN, and COL2A1 were measured via western blotting (n = 3). (C, D) The effects of TRIM38 knockdown on the levels of MMP-3, MMP-13, ACAN, and COL2A1 were assessed via western blotting (n = 3). **p < 0.01.

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