ADAMTS5 Antibody - #DF13268

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Product: ADAMTS5 Antibody
Catalog: DF13268
Description: Rabbit polyclonal antibody to ADAMTS5
Application: WB IHC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 72 kd; 102kD(Calculated).
Uniprot: Q9UNA0
RRID: AB_2846287

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MS Report
HPLC Report
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
ADAMTS5 Antibody detects endogenous levels of total ADAMTS5.
RRID:
AB_2846287
Cite Format: Affinity Biosciences Cat# DF13268, RRID:AB_2846287.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

A disintegrin and metalloproteinase with thrombospondin motifs 11; A disintegrin and metalloproteinase with thrombospondin motifs 5; A disintegrin like and metalloprotease (reprolysin type) with thrombospondin type 1 motif 5; A disintegrin like and metalloprotease (reprolysin type) with thrombospondin type 1 motif, 5 (aggrecanase 2); A disintegrin-like and metalloprotease with thrombospondin type 1 motif, 5; A Disintigrin And Metalloproteinase with ThromboSpondin motif-5; ADAM metallopeptidase with thrombospondin type 1 motif 5; ADAM TS 11; ADAM TS 5; ADAM TS5; ADAM-TS 11; ADAM-TS 5; ADAM-TS5; ADAMTS 11; ADAMTS 5; ADAMTS-11; ADAMTS-5; ADAMTS11; ADAMTS11, formerly; Adamts5; ADMP 2; ADMP-2; ADMP2; Aggrecanase 2; Aggrecanase-2; ATS5_HUMAN; FLJ36738; Implantin; ThromboSpondin motif-5;

Immunogens

Immunogen:
Uniprot:

Q9UNA0(ATS5_HUMAN) >>Visit HPA database.

Gene(ID):
ADAMTS5(11096)
Expression:
Q9UNA0 ATS5_HUMAN:

Expressed at low level in placenta primarily but also detected in heart and brain, cervix, uterus, bladder, esophagus, rib cartilage, chondroblastoma, fibrous tissue and a joint capsule from an arthritic patient.

Sequence:
MLLGWASLLLCAFRLPLAAVGPAATPAQDKAGQPPTAAAAAQPRRRQGEEVQERAEPPGHPHPLAQRRRSKGLVQNIDQLYSGGGKVGYLVYAGGRRFLLDLERDGSVGIAGFVPAGGGTSAPWRHRSHCFYRGTVDGSPRSLAVFDLCGGLDGFFAVKHARYTLKPLLRGPWAEEEKGRVYGDGSARILHVYTREGFSFEALPPRASCETPASTPEAHEHAPAHSNPSGRAALASQLLDQSALSPAGGSGPQTWWRRRRRSISRARQVELLLVADASMARLYGRGLQHYLLTLASIANRLYSHASIENHIRLAVVKVVVLGDKDKSLEVSKNAATTLKNFCKWQHQHNQLGDDHEEHYDAAILFTREDLCGHHSCDTLGMADVGTICSPERSCAVIEDDGLHAAFTVAHEIGHLLGLSHDDSKFCEETFGSTEDKRLMSSILTSIDASKPWSKCTSATITEFLDDGHGNCLLDLPRKQILGPEELPGQTYDATQQCNLTFGPEYSVCPGMDVCARLWCAVVRQGQMVCLTKKLPAVEGTPCGKGRICLQGKCVDKTKKKYYSTSSHGNWGSWGSWGQCSRSCGGGVQFAYRHCNNPAPRNNGRYCTGKRAIYRSCSLMPCPPNGKSFRHEQCEAKNGYQSDAKGVKTFVEWVPKYAGVLPADVCKLTCRAKGTGYYVVFSPKVTDGTECRLYSNSVCVRGKCVRTGCDGIIGSKLQYDKCGVCGGDNSSCTKIVGTFNKKSKGYTDVVRIPEGATHIKVRQFKAKDQTRFTAYLALKKKNGEYLINGKYMISTSETIIDINGTVMNYSGWSHRDDFLHGMGYSATKEILIVQILATDPTKPLDVRYSFFVPKKSTPKVNSVTSHGSNKVGSHTSQPQWVTGPWLACSRTCDTGWHTRTVQCQDGNRKLAKGCPLSQRPSAFKQCLLKKC

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

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

PTMs - Q9UNA0 As Substrate

Site PTM Type Enzyme
T36 O-Glycosylation
Y81 Phosphorylation
Y89 Phosphorylation
Y92 Phosphorylation
S208 O-Glycosylation
S214 O-Glycosylation
T215 O-Glycosylation
S440 Phosphorylation
S441 Phosphorylation
T444 Phosphorylation
N498 N-Glycosylation
W570 C-Glycosylation
W573 C-Glycosylation
S582 O-Glycosylation
K720 Ubiquitination
T746 Phosphorylation
K858 Acetylation
T899 Phosphorylation

Research Backgrounds

Function:

Metalloproteinase that plays an important role in connective tissue organization, development, inflammation, arthritis, and cell migration. ADAMTS5 is an extracellular matrix (ECM) degrading enzyme that show proteolytic activity toward the hyalectan group of chondroitin sulfate proteoglycans (CSPGs) including aggrecan, versican, brevican and neurocan. Cleavage within the hyalectans occurs at Glu-Xaa recognition motifs. Plays a role in embryonic development, including limb and cardiac morphogenesis, and skeletal muscle development through its versican remodeling properties. Participates in development of brown adipose tissue and browning of white adipose tissue. Plays an important role for T-lymphocyte migration from draining lymph nodes following viral infection.

PTMs:

The precursor is cleaved by furin and PCSK7 outside of the cell.

C- and O-glycosylated. O-fucosylated by POFUT2 on a serine or a threonine residue found within the consensus sequence C1-X(2)-(S/T)-C2-G of the TSP type-1 repeat domains where C1 and C2 are the first and second cysteine residue of the repeat, respectively. Fucosylated repeats can then be further glycosylated by the addition of a beta-1,3-glucose residue by the glucosyltransferase, B3GALTL. Fucosylation can mediate the efficient secretion of ADAMTS family members. Can be C-glycosylated with one or two mannose molecules on tryptophan residues within the consensus sequence W-X-X-W of the TPRs, and N-glycosylated. These other glycosylations can also facilitate secretion (By similarity).

Glycosylated. Can be O-fucosylated by POFUT2 on a serine or a threonine residue found within the consensus sequence C1-X(2)-(S/T)-C2-G of the TSP type-1 repeat domains where C1 and C2 are the first and second cysteine residue of the repeat, respectively. Fucosylated repeats can then be further glycosylated by the addition of a beta-1,3-glucose residue by the glucosyltransferase, B3GALTL. Fucosylation mediates the efficient secretion of ADAMTS family members. Also can be C-glycosylated with one or two mannose molecules on tryptophan residues within the consensus sequence W-X-X-W of the TPRs, and N-glycosylated. These other glycosylations can also facilitate secretion (By similarity).

Subcellular Location:

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
Tissue Specificity:

Expressed at low level in placenta primarily but also detected in heart and brain, cervix, uterus, bladder, esophagus, rib cartilage, chondroblastoma, fibrous tissue and a joint capsule from an arthritic patient.

Family&Domains:

The spacer domain and the TSP type-1 domains are important for a tight interaction with the extracellular matrix.

The conserved cysteine present in the cysteine-switch motif binds the catalytic zinc ion, thus inhibiting the enzyme. The dissociation of the cysteine from the zinc ion upon the activation-peptide release activates the enzyme.

References

1). Dual functions of microRNA-17 in maintaining cartilage homeostasis and protection against osteoarthritis. Nature Communications, 2022 (PubMed: 35508470) [IF=16.6]

Application: WB    Species: Mouse    Sample:

Fig. 2 miR-17 inhibits cartilage destruction by targeting multiple pathological catabolic factors. a Luciferase activity of 293 T cells co-transfected with dual-luciferase reporter constructs containing wild-type or mutated 3′-UTRs, as well as negative control (mimic NC) or miR-17 mimic. The data presented are mean percentage changes over mimic NC ± s.e.m. n = 6 biologically independent samples (NC + wt UTR, miR-17+wt UTR); n = 4 biologically independent samples (NC + mut UTR, miR-17 + mut UTR). b Mouse articular chondrocytes were transfected with miR-17 mimic (50 nM) or mimic NC and treated with or without IL-1β (5 ng/mL) for 24 h. The protein levels of catabolic and anabolic factors were determined by western blot followed by densitometry analysis. Blots are representative of three independent experiments. c, d qRT-PCR analysis of catabolic genes in knee cartilage (c), and representative images of IHC staining and quantification of MMP13+, ADAMTS5+ and NOS2+ cells in joint sections (d) of mice subjected to sham or DMM surgery and intra-articular injections of agomir-NC or agomir-17 (1.5 nmol) for 4 weeks, beginning at 4 weeks after surgery. n = 5 biologically independent samples per group in c. For MMP13 and ADAMTS5 staining, n = 4 mice (sham); n = 5 mice (DMM, DMM + agomir-17). For NOS2 staining, n = 4 mice per group. e, f qRT-PCR analysis of catabolic genes (e) and representative images of MMP13, ADAMTS5, and NOS2 immunostaining, and quantification of positive cells (f) from knee joints of cKO mice subjected to DMM surgery and intra-articular injection of agomir-NC, or agomir-17 (2 nmol). The injections were performed at 1 week after surgery and samples were collected at 2.5 weeks after surgery. n = 4 biologically independent samples per group in (e); n = 4 mice per group in (f). All scale bars, 100 μm. Data are presented as mean ± s.e.m. or boxplots (center line, median; box limits, 25 to 75th percentiles; whiskers, min to max), and dots represent individual mice or biologically independent samples. NS, not significant, *P < 0.05, **P < 0.01, and ***P < 0.001 in (a, c–f). *P < 0.05 versus control group, °P < 0.05 versus IL-1β + mimic NC in (b). Two-sided Student’s t test for (a); one-way ANOVA with Bonferroni’s test for (b–f). Exact P values in (b): *P = 0.0011, °P = 0.0205 (MMP3); *P <0.0001, °P = 0.0039 (MMP13); *P = 0.0015, °P = 0.0040 (ADAMTS5); *P = 0.0001, °P = 0.0013 (NOS2); *P = 0.0013, P > 0.9999 (SOX9); *P = 0.0001, P > 0.9999 (COL2A1). Source data are provided as a Source Data file.

Application: IHC    Species: Mouse    Sample:

Fig. 2 miR-17 inhibits cartilage destruction by targeting multiple pathological catabolic factors. a Luciferase activity of 293 T cells co-transfected with dual-luciferase reporter constructs containing wild-type or mutated 3′-UTRs, as well as negative control (mimic NC) or miR-17 mimic. The data presented are mean percentage changes over mimic NC ± s.e.m. n = 6 biologically independent samples (NC + wt UTR, miR-17+wt UTR); n = 4 biologically independent samples (NC + mut UTR, miR-17 + mut UTR). b Mouse articular chondrocytes were transfected with miR-17 mimic (50 nM) or mimic NC and treated with or without IL-1β (5 ng/mL) for 24 h. The protein levels of catabolic and anabolic factors were determined by western blot followed by densitometry analysis. Blots are representative of three independent experiments. c, d qRT-PCR analysis of catabolic genes in knee cartilage (c), and representative images of IHC staining and quantification of MMP13+, ADAMTS5+ and NOS2+ cells in joint sections (d) of mice subjected to sham or DMM surgery and intra-articular injections of agomir-NC or agomir-17 (1.5 nmol) for 4 weeks, beginning at 4 weeks after surgery. n = 5 biologically independent samples per group in c. For MMP13 and ADAMTS5 staining, n = 4 mice (sham); n = 5 mice (DMM, DMM + agomir-17). For NOS2 staining, n = 4 mice per group. e, f qRT-PCR analysis of catabolic genes (e) and representative images of MMP13, ADAMTS5, and NOS2 immunostaining, and quantification of positive cells (f) from knee joints of cKO mice subjected to DMM surgery and intra-articular injection of agomir-NC, or agomir-17 (2 nmol). The injections were performed at 1 week after surgery and samples were collected at 2.5 weeks after surgery. n = 4 biologically independent samples per group in (e); n = 4 mice per group in (f). All scale bars, 100 μm. Data are presented as mean ± s.e.m. or boxplots (center line, median; box limits, 25 to 75th percentiles; whiskers, min to max), and dots represent individual mice or biologically independent samples. NS, not significant, *P < 0.05, **P < 0.01, and ***P < 0.001 in (a, c–f). *P < 0.05 versus control group, °P < 0.05 versus IL-1β + mimic NC in (b). Two-sided Student’s t test for (a); one-way ANOVA with Bonferroni’s test for (b–f). Exact P values in (b): *P = 0.0011, °P = 0.0205 (MMP3); *P <0.0001, °P = 0.0039 (MMP13); *P = 0.0015, °P = 0.0040 (ADAMTS5); *P = 0.0001, °P = 0.0013 (NOS2); *P = 0.0013, P > 0.9999 (SOX9); *P = 0.0001, P > 0.9999 (COL2A1). Source data are provided as a Source Data file.
2). Pentraxin 3 regulated by miR-224-5p modulates macrophage reprogramming and exacerbates osteoarthritis associated synovitis by targeting CD32. Cell Death & Disease, 2022 (PubMed: 35739102) [IF=9.0]

Application: IF/ICC    Species: Mouse    Sample:

Fig. 2 PTX3 accelerates synovitis, cartilage erosion, and exacerbates OA development in mice. A, B Safranin O/fast green staining and Osteoarthritis Research Society International (OARSI) grades of knee cartilage from DMM mice treated with vehicle, recombinant mouse PTX3 (rmPTX3), or PTX3 neutralizing antibody (PTX3-NAb) for 4 weeks and 8 weeks. Scale bar: 100 µm. C–F IF staining and quantification of ADATMS5 and MMP13 in knee cartilage of controls and DMM mice treated with vehicle, rmPTX3, or PTX3-NAb for 8 weeks. Scale bar: 50 µm. G IF staining and quantification of COL2 in knee cartilage of controls and DMM mice treated with rmPTX3 or PTX3-NAb for 8 weeks. Scale bar: 50 µm. H, I H&E and synovitis score of synovial tissues from DMM mice treated with vehicle, rmPTX3, or PTX3-NAb for 4 weeks and 8 weeks. Scale bar: 100 µm. *P 
3). 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: WB    Species: Human    Sample: C28/I2 cells

Fig. 4. Knockdown of FOXO3a compromised the inhibitory effects of TMF on C/EBPβ-mediated ECM degradation. (A–B) IHC assays were used to detect the altered expression of FOXO3a. (C–D) The protein expression of FOXO3a in shRNA-FOXO3a-infected C28/I2 cells was detected by western blotting assays. (E–K) Western blotting assays were used to detect the protein expression of Aggrecan, ADAMTS5, C/EBPβ, p-C/EBPβ, caspase3, cleaved-caspase3, and FOXO3a in LV-sh-FOXO3a-infected C28/I2 cells treated with IL-1β. (L-M) The apoptosis rate was determined by a flow cytometer.
4). The Protective Effect of Evodiamine in Osteoarthritis: An In Vitro and In Vivo Study in Mice Model. Frontiers in Pharmacology, 2022 (PubMed: 35795554) [IF=5.6]

Application: WB    Species: Mouse    Sample:

FIGURE 4 Evodiamine had a protective effect on the ECM degradation of IL-1β–induced chondrocytes. (A,B,C,D) Relative protein expressions of collagen-II, ADAMTS-5, and MMP-13 were quantitated by Western blot. (E,F) Collagen-II (green) was detected by immunofluorescence. Data were expressed as mean ± SD. Significant differences between different groups are indicated as ##p < 0.01, vs. control group; ∗∗ p < 0.01, vs. IL-1β alone stimulation group, n = 3.
5). Casticin ameliorates osteoarthritic cartilage damage in rats through PI3K/AKT/HIF-1α signaling. Chemico-biological interactions, 2024 (PubMed: 38309612) [IF=5.1]
6). Medical Prospect of Melatonin in the Intervertebral Disc Degeneration through Inhibiting M1-Type Macrophage Polarization via SIRT1/Notch Signaling Pathway. Biomedicines, 2023 (PubMed: 37371708) [IF=4.7]

Application: WB    Species: Human    Sample: NP cells

Figure 4 Protection on NP cells against the CM-induced inflammation and imbalanced ECM homeostasis by the treatment of MLT. NP cells were treated with different CMs collected from the LPS-stimulated RAW 264.7 Mφs in the presence or absence of MLT for 24 h, then followed by different analysis. (A) The relative mRNA levels of pro-inflammation cytokines in NP cells were measured by RT-qPCR analyses (n = 3). The levels of IL-6, TNF-α, iNOS and COX-2 mRNA declined in the presence of MLT treatment to Mφs at different dosages. (B) The relative mRNA levels of matrix anabolic and degrading enzymes in NP cells were measured by RT-qPCR analyses (n = 3). The levels of COL2A1 and TIMP-1 mRNA were upregulated, while the levels of MMP-13, ADAMTS4 and ADAMTS5 mRNA were downregulated in the presence of MLT treatment to Mφs at different dosages. (C,D) The relative protein levels of pro-inflammation cytokines in NP cells were measured by Western blot analyses (n = 3). (C) Western blotting showed the decline of inflammation-associated proteins. (D) Quantitative analysis showed the reduced levels of IL-6, TNF-α, iNOS and COX-2 protein after treatment with MLT to Mφs at different dosages. (E,F) The relative protein levels of matrix anabolic and degrading enzymes in NP cells were measured by Western blot analyses (n = 3). (E) Western blotting showed the different changes of ECM protein productions in NP cells. (F) Quantitative analysis showed the increased levels of COL2A1 and TIMP-1 protein, and the reduced levels of MMP-13, ADAMTS4 and ADAMTS5 protein after the treatment with MLT to Mφs at different dosages. Data are expressed as mean ± standard deviation. The two groups among the five groups are compared by using an independent t-test.
7). Resveratrol protection against IL-1β-induced chondrocyte damage via the SIRT1/FOXO1 signaling pathway. Journal of Orthopaedic Surgery and Research, 2022 (PubMed: 36064420) [IF=2.6]
8). Programmed NP Cell Death Induced by Mitochondrial ROS in a One-Strike Loading Disc Degeneration Organ Culture Model. Oxidative Medicine and Cellular Longevity, 2021 (PubMed: 34512867)

Application: IF/ICC    Species: Human    Sample: NP tissue

Figure 5 Mitochondrial ROS participated in MS-mediated metabolic dysregulation. Gene expression was analyzed by RT-qPCR for (a) MMP1, (b) MMP3, (c) MMP13, (d) ADAMTS4, (e) ADAMTS5, and (f) COL2A1. The gene expression levels in the MS group and the MitoQ + MS group are expressed relative to those in the CON group at 12 hours after MS. The expression levels in the MS 7-day group were similar to those in the CON 7-day group. The data are expressed as the means ± SEMs. n = 5. (g–j) Anabolic-related markers and collagen II in NP tissue were examined using immunohistochemical staining. Scale bars, 50 μm and 5 μm (inset). n = 3. (k) Cumulative release of GAG into a culture medium. n = 3. The data are expressed as the means ± SEMs. ∗P < 0.05 and ∗∗P < 0.01.

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