MA1-37493

antibody from Invitrogen Antibodies

Targeting: COL2A1 AOM, SEDC, STL1

Provider product page for MA1-37493

Western blot

Immunohistochemistry

Flow cytometry

Other assay

Antibody data

Antibody Data
Antigen structure
References [72]
Comments [0]
Validations
Other assay [15]

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Product number: MA1-37493 - Provider product page
Provider: Invitrogen Antibodies
Product name: Collagen II Monoclonal Antibody (2B1.5)
Antibody type: Monoclonal
Antigen: Purifed from natural sources
Description: Staining of formalin/parafin tissues requires disgestion of tissue sections with pepsin at 1 mg/mL Tris-HCl, pH 2.0 for 15 min at RT or 10 min at 37C.
Reactivity: Human, Mouse, Rat, Bovine, Chicken/Avian
Host: Mouse
Isotype: IgG
Antibody clone number: 2B1.5
Vial size: 200 µg
Concentration: 0.2 mg/mL
Storage: 4° C

COL2A1 protein structure - MA1-37493 shown in red.

Supportive validation

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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 4. Effect of AG on IL-1beta-induced extracellular matrix degradation in human NP cells. NP cells were stimulated by IL-1beta with or without AG treatment. Immunofluorescence images of (A) collagen-II and (B) aggrecan expression following treatment (magnification, x400). (C) The protein expression levels of aggrecan and collagen were determined western blot analysis. (D) Quantification of collagen levels. (E) Quantification of aggrecan levels. The values are presented as the mean +- standard deviation of 3 independent experiments. *P

Supportive validation

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Experimental details: FIGURE 2 Cells in the cartilaginous anlagen are the major contributors to epiphyseal cartilage development in an asymmetrical manner. (A-H) Example images illustrating the distribution of traced Col2-expressing clones in the epiphyseal cartilage of knee joint. D, I, and V refer to dorsal condyle, intercondylar eminence, and ventral condyle regions, respectively. (I-L) 1-day tracings of the Col2-expressing cells from E12.5 to E13.5 and E13.5 to E14.5 mainly labeled the cells in the diaphyseal side of the cartilaginous anlagen. (J) and (L) are alcian blue and eosin staining of the same tissue section on the left. (M) Quantification of the clonal density distribution revealed an ascending trend in the epiphyseal cartilage among the four tracing periods. (N,O) Quantification of the clonal density distribution in the D, I, and V regions revealed an asymmetrical contribution of the Col2-expressing clones to the femoral and tibial epiphyseal cartilage along the dorsal-ventral axis during many of the analyzed tracing periods. Clonal density represents the number of traced clones over cartilage area (mm 2 ). Data represent mean +- SEM, where at least five embryos were analyzed. The white dashed lines outline the epiphyseal and diaphyseal cartilage (DC). * P < 0.05, ** P < 0.01, **** P < 0.001, ns, not significant.

Supportive validation

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Experimental details: Figure 2 Downregulation of Cx43 by oleuropein decreases GJIC and improves the phenotype of OACs. ( A ) Oleuropein (Oleu) treatment significantly decreases GJIC evaluated by an SL/DT assay when OACs were exposed with this molecule for 2 h (top, n=6 independent experiments; Student's t test, P

Supportive validation

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Experimental details: Figure 3 Oleuropein treatment enhances chondrocyte redifferentiation. ( A ) Immunohistochemistry of Col2A1 (4-6 independent experiments; one-way ANOVA, P =0.0019) and toluidine blue staining of proteoglycan subunits (n=6 independent experiments; one-way ANOVA, P =0.059) indicate significant enrichment in ECM components in OACs micromasses grown in 3D culture for 30 days in chondrogenic medium (CM) when supplemented with 10 muM oleuropein (Oleu) or OE. ( B ) Cx43 protein levels detected by western blot (and normalized to Ponceau staining) are reduced when OACs micromasses are exposed to CM supplemented with 10 muM oleuropein or OE for 21 days (n=3 independent experiments; one-way ANOVA, P =0.0328). ( C ) Oil red staining showing reduced OACs dedifferentiation upon exposure to Oleu or OE in adipogenic medium (n=5 independent experiments; one-way ANOVA, P =0.0001). ( D ) Nuclear levels of Twist-1 were decreased in OACs cultured with 10 muM oleuropein for 2 h. Lamin A was used as a loading control (n=3 independent experiments; Student's t test, P =0.001). ( E ) Cx43 protein levels in primary OACs after 1-h treatment with oleuropein or oligomycin. Western blot represents n=4 independent experiments. Quantification is shown on the right (one-way ANOVA, P =0.0036). On the right, immunofluorescence for Twist-1 (red) in primary OACs treated with 5 mug/mL oligomycin and 10 muM oleuropein for 1 h. The graph represents the percentage of cells with Twist-1 nuclear localization (n=4 indepe

Supportive validation

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Experimental details: Fig. 1 OAC reverts to a more progenitor-like or stem cell-like phenotype. a Mesenchymal stem cell markers (CD90, CD105, CD29, CD44, CD166 and CD73) were tracked by flow cytometry for 7 and 14 days during chondrogenic differentiation of hMSCs in monolayer culture. Data were normalized to the 0-day value. b Dedifferentiation of OAC to a more progenitor-like cell state at different time periods in monolayer culture was quantified with the same stem cell markers and flow cytometry. Data were normalized to those of low passage numbers (

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 2 Downregulation of Cx43 GJ plaques and GJIC restores chondrocyte redifferentiation in chondrocytes from patients with OA. a OACs express higher levels of Cx43 protein (mainly located in GJ plaques, white arrows) compared with chondrocytes from healthy donors (N), (western blot, flow cytometry and immunofluorescence assays ( n = 3; mean +- s.e.m.; * P < 0.05; Mann-Whitney test). b OACs show higher levels of GJIC in comparison with healthy chondrocytes in primary cultures measured by SL/DT assay ( n = 3; mean +- s.e.m.; * P < 0.05; Mann-Whitney test). c Flow cytometry analysis shows reduced levels of CD105 and CD166 in OACs treated for 7 days with 100 uM CBX, suggesting reduced chondrocyte dedifferentiation upon GJIC inhibition. Graphs show CD105 and CD166 levels detected in OACs exposed to CBX or chondrogenic medium (CM) ( n = 4-5; mean +- s.e.m.; * P < 0.05, ** P < 0.01, *** P < 0.0001; one-way ANOVA). d OACs in chondrogenic (CM) and normal growth medium (UT, DMEM 10% FBS) for 48 h. GJCI was measured by SL/DT assay ( n = 3; mean +- s.e.m.; *** P < 0.0001; Mann-Whitney test). e CBX 50 and 100 uM inhibit GJIC in OACs measured by SL/DT assay (Supplementary Fig. 3a ). Immunofluorescence analysis of Col2A1 and Cx43 levels in OACs treated with CBX 50 and 100 uM for 24 h. The graphs show the percentage of positive cells for Col2A1 and the CTCF for Cx43 mainly located in the margin of the cells (gap junction plaques, white arrows) ( n = 5; mean +- s.e.m.; *