MA5-13188

antibody from Invitrogen Antibodies

Targeting: PECAM1 CD31

Provider product page for MA5-13188

Western blot

Antibody data

Antibody Data
Antigen structure
References [90]
Comments [0]
Validations
Western blot [2]
Immunocytochemistry [2]
Immunohistochemistry [1]
Flow cytometry [1]
Other assay [14]

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Product number: MA5-13188 - Provider product page
Provider: Invitrogen Antibodies
Product name: CD31 Monoclonal Antibody (JC/70A)
Antibody type: Monoclonal
Antigen: Other
Description: MA5-13188 targets CD31 in ICC/IF, FACS, WB and IHC (P) applications and shows reactivity with Human samples.
Antibody clone number: JC/70A
Concentration: 0.2 mg/mL

PECAM1 protein structure - MA5-13188 shown in red.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunofluorescent analysis of CD31 (green) showing staining in the cytoplasm and membrane of THP-1 cells (right) compared to a negative control without primary antibody (left). Formalin-fixed cells were permeabilized with 0.1% Triton X-100 in TBS for 5-10 minutes and blocked with 3% BSA-PBS for 30 minutes at room temperature. Cells were probed with a CD31 monoclonal antibody (Product # MA5-13188) in 3% BSA-PBS at a dilution of 1:20 and incubated overnight at 4 ºC in a humidified chamber. Cells were washed with PBST and incubated with a DyLight-conjugated secondary antibody in PBS at room temperature in the dark. F-actin (red) was stained with a fluorescent red phalloidin and nuclei (blue) were stained with Hoechst or DAPI. Images were taken at a magnification of 60x.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunofluorescence analysis of Platelet endothelial cell adhesion molecule was performed using 70% confluent log phase HUVEC cells. The cells were fixed with 4% paraformaldehyde for 10 minutes, permeabilized with 0.1% Triton™ X-100 for 15 minutes, and blocked with 2% BSA for 45 minutes at room temperature. The cells were labeled with CD31 Monoclonal Antibody (JC/70A) (Product # MA5-13188) at 1:100 dilution in 0.1% BSA, incubated at 4 degree celsius overnight and then labeled with Donkey anti-Mouse IgG (H+L) Highly Cross-Adsorbed Secondary Antibody, Alexa Fluor Plus 488 (Product # A32766), (1:2000 dilution), for 45 minutes at room temperature (Panel a: Green). Nuclei (Panel b: Blue) were stained with ProLong™ Diamond Antifade Mountant with DAPI (Product # P36962). F-actin (Panel c: Red) was stained with Rhodamine Phalloidin (Product # R415, 1:300 dilution). Panel d represents the merged image showing Cell Junctional localization. Panel e represents no expression in MDA-MB-231. Panel f represents control cells with no primary antibody to assess background. The images were captured at 60X magnification.

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: Fig 6 Photomicrographs of the skin wound area, day 10. (a) Control group, showing mild localized immunoreactivity in the endothelial cells of dermal blood vessels (arrows). (b) Group II showing moderate immunoreactivity. (c,d) Group III and IV showing dense immunoreactivity in the endothelial cells of dermal blood vessels (arrows). By day 15: (e,f,g) Control, Group II and III showing mild localized immunoreactivity in the endothelial cells of dermal blood vessels (arrows). (h) Group IV showing absence of immunoreactivity in the healed wound area. (CD 31; x 400)

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 6 EMPs are taken up by normal cells. ( A ) Cells were incubated with an equal concentration of CFSE-EMPs (green), then fixed (but not permeabilized) and stained with anti-CD31 to outline the plasma, and visualized using confocal microscopy after 1/2h,15h. (Bars=5mum) ( B ) Differential uptake of HG-EMPs and control-EMPs by normal HUVECs. All data were expressed as means +- SEM (Four fields of view are randomly selected for each group. Bars represent the SEM from four independent experiments).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 8 mTORC1-STAT3-FGFBP1 pathway regulates angiogenesis in an OVA-induced chronic asthma model. A The timeline to establish OVA-induced chronic asthma models and therapeutic interventions (see the ""Materials and methods"" section for details). The mice were divided into three groups: the control group (Control), OVA-induced chronic asthma group (OVA), and rapamycin-treated group (Rapa). B The total number of leukocytes and eosinophil count in the BALF were counted using Wright-Giemsa staining. C Representative photographs of H&E staining (upper panels) and Masson's staining (lower panels) of lung tissues (scale bar: 100 mum). D Inflammation score (left panels) and Wat/Pbm (right panels) of lung tissues. E Immunoblotting of the indicated proteins in lung tissues. F IHC analysis of the indicated proteins in lung tissues (scale bar: 100 mum). n = 8 mice per group. Results are shown as mean +- SD. ** P < 0.01; *** P < 0.001; **** P < 0.0001. G Schematic illustration of activated mTORC1-STAT3-FGFBP1 signaling pathway promotes angiogenesis in airway epithelial cells.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: FIGURE 6 Tissue processing to assess viability and biointegration. (A) Tissue is prepared for 3D-ST resection beginning at the closure site; (B) 3D-ST implantation site identified using surgical details documented at the time of surgery; (C) ligation surgical clips were separated from the resected tissue; (D) specimens were embedded in OCT and (E) cyrosectioned for immunohistochemistry; (F) Live/Dead assays of time-matched in vitro controls; scale bar = 25 mum and (G) resected tissue 8 weeks post-surgery; scale bar = 25 mum. (H) Plasma and saliva collections are used for human alpha-amylase and GLuc detection; (I-J) visualization of resected tissue revealed tissue response (blue nuclei) to surgical sutures; scale bar = 100 mum. (K) Vasculature (CD31, green) and human alpha-amylase (red, white arrow) adjacent to 3D-ST in serial cryosection of human nuclear antigen (HNA + ) structures ~256 mum away; scale bar = 25 mum. (L) Human nuclear antigen antibody (HNA, green; scale bar = 25 mum) validated using human parotid tissue was (M) present in structures in resected implant tissue after 4 weeks; scale bar = 100 mum. (N) Nerve fibers in tissue adjacent to implant, ~448 mum away from HNA + structures, was shown by the presence of beta-III tubulin (green) staining traversing the tissue; scale bar = 100 mum.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 1 Formation of in-vitro vascularized breast cancer tissue. ( a ) Morphology of GFP + MDA-MB231 (green) in 2-D cell culture plate, Scale = 100 um, ( b ) morphology of GFP + MDA-MB231 embedded in scaffold-free vascularized tissue, vessels were stained (grey) with PECAM1 (CD-31), Scale = 100 um, ( c ) highly elongated BCCs filopodia observed in 3-D tissues wrapped around a vessel branch, Scale = 100 um, ( d ) direct interaction between cancer cells and BVs, orthogonal projections are shown, ( e ) pictorial representation of the change of morphology of MDA-MB231 in 2-D culture and 3-D scaffold-free culture, ( f ) cell aspect ratio in 2-D is in the lower range as compared to cells in the 3-D models that range from low to high (data from randomly selected 20 cells from 3 samples), ( g ) cell circularity (1 = circular, 0 = elongated) analysis show that cells in 3-D tend to be more elongated as compared to 2-D cultures (randomly selected 20 cells from 3 samples).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Representative staining images of regenerated tissue at week 12. a1 H&E staining of regenerated bones induced by different scaffolds at week 12 after operation. a2 Masson's trichrome staining at week 12 after the operation. a3 CD31 immunofluorescence staining of regenerated vessels at week 12. (Row 1: Overall observation of the cranial defect repair. The red arrow indicates the initial boundary of the defect. Row 2: Magnified view of the center and boundary site of the defects). (N: new bone tissue. S: scaffolds. V: new blood vessels (black arrow). F: fibrous tissue. B: old bone boundary). b1 - 4 Representative immunohistochemistry images of BMP-2, Runx2, OCN, VEGF at week 12 after implantation. c Quantitative analysis of positive cells at week 12. (all scaffolds without cells. Blank: defect alone with no treatment) (*** p = 3.7616 x 10 -5 , * p = 0.0114; *** p = 2.1035 x 10 -5 , ** p = 0.0032, *** p = 6.41247 x 10 -5 , * p = 0.0355, *** p = 5.2544 x 10 -5 , * p = 0.0409). (Two-sided comparison, error bars represent standard deviation, * p < 0.05, ** p < 0.01, and *** p < 0.001).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: The angiogenic sprouting in all three culture conditions. The immunofluorescence images with F-actin signal of (A) the obstructing condition, (B) the soaking condition, and (C) the flowing condition (green: F-actin, blue: Nuclei, scale bar: 100 mum). The immunofluorescence images with CD31 signal of (D) the obstructing condition, (E) the soaking condition, and (F) the flowing condition (green: CD31, blue: Nuclei, scale bar: 100 mum). (G) The sprouting number was graphed. (H) The average length of the sprout was analyzed.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 7 (a-d) Representative images of PECAM1 IHC staining of newborn laminae in the CSFP group and the Non-CSFP group at the 4 th and 8 th weeks. (e) The PECAM1 IHC staining of the paraspinal surface of the newborn laminae in the 12 th week. (f) The PECAM1 IHC staining of the dural surface of the newborn laminae in the 12 th week. (g) Quantification of PECAM1 expression by IHC staining. (h) QRT-PCR analysis of PECAM1 expressions. The red arrow showed positive staining. The dashed line in images (a), (b), and (f) showed the vertebral canal. The dashed line in images (c) showed the outer cortex of native laminae.