MA5-13398

antibody from Invitrogen Antibodies

Targeting: THBS1 THBS, THBS-1, TSP, TSP-1, TSP1

Provider product page for MA5-13398

Western blot

Antibody data

Antibody Data
Antigen structure
References [149]
Comments [0]
Validations
Western blot [1]
Immunocytochemistry [3]
Immunohistochemistry [4]
Flow cytometry [4]
Other assay [25]

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Product number: MA5-13398 - Provider product page
Provider: Invitrogen Antibodies
Product name: Thrombospondin 1 Monoclonal Antibody (A6.1)
Antibody type: Monoclonal
Antigen: Purifed from natural sources
Description: MA5-13398 targets Thrombospondin in FACS, ICC/IF, IHC (P), IM, IP, and WB applications and shows reactivity with Bovine, Canine, Equine, Human, mouse, Ovine, Porcine, and Rat samples.
Antibody clone number: A6.1
Concentration: 0.5 mg/mL

THBS1 protein structure - MA5-13398 shown in red.

Supportive validation

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Experimental details: Immunofluorescent analysis of Thrombospondin (green) showing staining in the secretion of HeLa cells. 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 Thrombospondin monoclonal antibody (Product # MA5-13398) in 3% BSA-PBS at a dilution of 1:100 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

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Experimental details: Immunofluorescent analysis of Thrombospondin (green) showing staining in the secretion of HepG2 cells. 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 Thrombospondin monoclonal antibody (Product # MA5-13398) in 3% BSA-PBS at a dilution of 1:100 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

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Experimental details: Immunofluorescent analysis of Thrombospondin (green) showing staining in the secretion of NIH-3T3 cells. 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 Thrombospondin monoclonal antibody (Product # MA5-13398) in 3% BSA-PBS at a dilution of 1:100 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

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Experimental details: Formalin-fixed, paraffin-embedded human placenta stained with Thrombospondin antibody using peroxidase-conjugate and AEC chromogen. Note staining of platelets in the blood vessels.

Supportive validation

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Experimental details: Immunohistochemistry analysis of Thrombospondin showing positive staining in the Extracellular and platelet A-granules of paraffin-treated Human placenta tissue (right) compared with a negative control in the absence of primary antibody (left). To expose target proteins, antigen retrieval method was performed using 10mM sodium citrate (pH 6.0) microwaved for 8-15 min. Following antigen retrieval, tissues were blocked in 3% H2O2-methanol for 15 min at room temperature, washed with ddH2O and PBS, and then probed with a Thrombospondin monoclonal antibody (Product # MA5-13398) diluted by 3% BSA-PBS at a dilution of 1:20 overnight at 4°C in a humidified chamber. Tissues were washed extensively PBST and detection was performed using an HRP-conjugated secondary antibody followed by colorimetric detection using a DAB kit. Tissues were counterstained with hematoxylin and dehydrated with ethanol and xylene to prep for mounting.

Supportive validation

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Experimental details: Immunohistochemistry analysis of Thrombospondin showing positive staining in the Extracellular and platelet A-granules of paraffin-treated Human tonsil tissue (right) compared with a negative control in the absence of primary antibody (left). To expose target proteins, antigen retrieval method was performed using 10mM sodium citrate (pH 6.0) microwaved for 8-15 min. Following antigen retrieval, tissues were blocked in 3% H2O2-methanol for 15 min at room temperature, washed with ddH2O and PBS, and then probed with a Thrombospondin monoclonal antibody (Product # MA5-13398) diluted by 3% BSA-PBS at a dilution of 1:20 overnight at 4°C in a humidified chamber. Tissues were washed extensively PBST and detection was performed using an HRP-conjugated secondary antibody followed by colorimetric detection using a DAB kit. Tissues were counterstained with hematoxylin and dehydrated with ethanol and xylene to prep for mounting.

Supportive validation

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Main image
Experimental details: Immunohistochemistry analysis of Thrombospondin showing positive staining in the Extracellular and platelet A-granules of paraffin-treated Mouse lung tissue (right) compared with a negative control in the absence of primary antibody (left). To expose target proteins, antigen retrieval method was performed using 10mM sodium citrate (pH 6.0) microwaved for 8-15 min. Following antigen retrieval, tissues were blocked in 3% H2O2-methanol for 15 min at room temperature, washed with ddH2O and PBS, and then probed with a Thrombospondin monoclonal antibody (Product # MA5-13398) diluted by 3% BSA-PBS at a dilution of 1:20 overnight at 4°C in a humidified chamber. Tissues were washed extensively PBST and detection was performed using an HRP-conjugated secondary antibody followed by colorimetric detection using a DAB kit. Tissues were counterstained with hematoxylin and dehydrated with ethanol and xylene to prep for mounting.

Supportive validation

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Experimental details: Flow cytometry analysis of Thrombospondin in Hela cells compared to an isotype control (blue). Cells were harvested, adjusted to a concentration of 1-5x10^6 cells/mL, fixed with 2% paraformaldehyde, washed with PBS, and incubated with Thrombospondin monoclonal antibody (Product # MA5-13398) at a dilution of 0.5 µg/test for 60 min at room temperature. Cells were then blocked in a solution of 2% BSA-PBS for 30 min at room temperature, incubated for 40 min at room temperature in the dark using a Dylight 488-conjugated goat anti-mouse IgG (H+L) secondary antibody, and re-suspended in PBS for FACS analysis.

Supportive validation

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Main image
Experimental details: Flow cytometry analysis of Thrombospondin in Hela cells compared to an isotype control (blue). Cells were harvested, adjusted to a concentration of 1-5x10^6 cells/mL, fixed with 2% paraformaldehyde, washed with PBS, and incubated with Thrombospondin monoclonal antibody (Product # MA5-13398) at a dilution of 0.5 µg/test for 60 min at room temperature. Cells were then blocked in a solution of 2% BSA-PBS for 30 min at room temperature, incubated for 40 min at room temperature in the dark using a Dylight 488-conjugated goat anti-mouse IgG (H+L) secondary antibody, and re-suspended in PBS for FACS analysis.

Supportive validation

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Experimental details: Flow cytometry analysis of Thrombospondin in HepG2 cells compared to an isotype control (blue). Cells were harvested, adjusted to a concentration of 1-5x10^6 cells/mL, fixed with 2% paraformaldehyde, washed with PBS, and incubated with Thrombospondin monoclonal antibody (Product # MA5-13398) at a dilution of 0.5 µg/test for 60 min at room temperature. Cells were then blocked in a solution of 2% BSA-PBS for 30 min at room temperature, incubated for 40 min at room temperature in the dark using a Dylight 488-conjugated goat anti-mouse IgG (H+L) secondary antibody, and re-suspended in PBS for FACS analysis.

Supportive validation

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Experimental details: Flow cytometry analysis of Thrombospondin in L929 cells compared to an isotype control (blue). Cells were harvested, adjusted to a concentration of 1-5x10^6 cells/mL, fixed with 2% paraformaldehyde, washed with PBS, and incubated with Thrombospondin monoclonal antibody (Product # MA5-13398) at a dilution of 0.5 µg/test for 60 min at room temperature. Cells were then blocked in a solution of 2% BSA-PBS for 30 min at room temperature, incubated for 40 min at room temperature in the dark using a Dylight 488-conjugated goat anti-mouse IgG (H+L) secondary antibody, and re-suspended in PBS for FACS analysis.

Supportive validation

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Supportive validation

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Supportive validation

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Experimental details: Immunoprecipitation of Thrombospondin using Thrombospondin Monoclonal Antibody (Product # MA5-13398) on Native Human HUVEC Cells.

Supportive validation

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Experimental details: FIGURE 5. Efb interacts with platelet P-selectin. A , human platelets were ultrasonicated in the presence or absence of 3 mg/ml added fibrinogen. Sigma His-Select HF nickel affinity gel was used to capture His-tagged Efb- or Efb-N-interacting proteins from platelet lysates. Affinity precipitates were separated by SDS-PAGE and immunoblotted for integrin alphaIIb, P-selectin, multimerin-1, fibronectin, thrombospondin-1 (indicated by Thrombosp.-1 ), and His tag (to confirm Efb/Efb-N expression and immobilization). Immunoblots shown here are representative of those from three independent experiments. -ve , negative control; PD , pulldown. B , SPR data confirm the direct interaction of Efb and P-selectin. Recombinant P-selectin-Fc immobilized on COOHV-coated SensiQ TM sensor chips was treated with increasing concentrations of Efb (100 n m ( brown ), 300 n m ( purple ), and 2.8 mu m ( green )). All experiments were performed using the SensiQ TM Pioneer FE SPR platform (SensiQ Technologies). Experimental data were fit using the Qdat data analysis software. Curves were fitted using a least squares fitting algorithm. RU , response units.

Supportive validation

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Experimental details: Figure 3 Analysis of miRNA targets. (A) Venn diagram summarizing the rationale for selecting putative miRNA targets by combining the lists generated with prediction algorithms with those generated from expression datasets (1,858 genes with a fold change

Supportive validation

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Experimental details: Fig 3 Alterations to VEGF-A and TSP-1 with elevated CORT and concomitant prazosin treatment. RNA or protein was isolated from the TA muscle after 1W or 2W of CORT with or without concurrent prazosin treatment. Taqman qPCR was used to assess the mRNA levels of VEGF-A (A,B) and TSP-1 (D,E), while VEGF-A protein was assessed by ELISA (C) and TSP-1 protein by Western blot (F). (A) VEGF-A mRNA was not altered in response to 1W CORT and/or prazosin. (B) VEGF-A mRNA was not affected by 2W CORT ( P = 0.08), while a significant prazosin effect was detected within the 2W CORT-prazosin group (* P

Supportive validation

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Experimental details: Figure 3 High glucose treatment shifted endothelial cell angiomiR expression towards an anti-angiogenic phenotype. ( A ) Primary miR and ( B ) mature miR levels relative to HPRT housekeeping gene and exogenous spike-in cel-miR-39-3p, respectively. Pro-angiogenic pri-miRs and miR are underlined in red, while angiostatic pri-miRs and miRs are underlined in blue. Data are means +- SEM ( n = 6). Two-way ANOVA showed no effect of glucose concentration on the expression of pri-miR-126, pri-miR-17-92, and pri-miR-15; *** indicates significative difference compared to 5 mM of glucose ( p < 0.001)). ( C , D ) VEGF-A and THBS-1 mRNA relative to HPRT in HDMEC treated with 5 or 30 mM glucose concentrations for 24 h (data are means +- SEM, n = 9). ( E , F ) Immunoblots of miR targets VEGF-A and THBS-1 (A6.1) after 24 h treatment under 5 or 30 mM glucose conditions. alpha,beta-TUBULIN was used as a loading control. Data are means +- SEM; * indicates significative differences ( p < 0.05, t -test, n = 5-10).

Supportive validation

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Experimental details: Figure 6 MT 1- MMP absence in endothelial cells leads to perivascular accumulation of thrombospondin-1 ( TSP 1) in the inflamed colon A, B Representative maximum-intensity projection images of staining for TSP1 (red) and CD31 (gray) in (A) and also for MT1-MMP (green) in (B) in colon sections obtained from MT1 f/f and MT1 iDeltaEC mice left untreated (A) or treated with 1% DSS for 3 days (B). Magnified views are shown to the right. Scale bars, 100 mum in main panels and 10 mum in the magnified views. C TSP1 mean fluorescence intensity (MFI) in the perivascular area of large vessels present in the colon mucosa of treated mice, as depicted in (B); n = 4 mice per genotype. Data are shown as mean +- SEM and were tested by t -test; * P < 0.05. Data information: Please see Appendix Table S3 for exact P -values. Source data are available online for this figure.

Supportive validation

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Experimental details: Figure 2 MTRN localization in non-human primate retina flat-mount. Immunostaining on the flat-mount retina of MTRN (green), TSP1 (red), and GS (red). MTRN and TSP1 are highly concentrated around the optic nerve head (NO = Optic Nerve), and co-localize at the macula and around the fovea* ( a ). Colocalization of MTRN with GS expressed in Muller cells at the macula ( b and inset).

Supportive validation

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Experimental details: Figure 4 Human immunostaining of MTRN and TSP1 on retinal cryosection. Immunostaining on human retinal cryosection of MTRN (green), TSP1 (red), counter marked with DAPI (blue). MTRN (green) colocalized in all layers with TSP1, in macula ( a ) and is expressed in the cytoplasm and in nuclei of ganglion cells, in nuclei of inner and outer layers (INL, ONL) (b), in Muller fibers ( c ), and in the inner segment of photoreceptors ( d ). Close to the optic nerve, MTRN is strongly present in nerves fibers ( e ), in Bruch's membrane (BM) ( f ). MTRN is also found as a gradient starting from the BM towards the deeper choroidal vessels ( f ).

Supportive validation

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Experimental details: Figure 7 MTRN effect on CNV quantified by isolectin B4. Choroidal flat-mount laser impact images, for each treatment, stained with ss4-isolectin (green) ( a ). Quantification of neovascular volume ( b ). Immunostaining of isoLB4 (green), GFAP (red), and TSP1 (purple) on neuroretina treated by PBS ( c , d and insets) and MTRN ( g , h and insets), and on laser impacts of RPE-choroid complex treated by PBS ( e , f ) and MTRN ( i,j ). * ( p = 0.03), ** ( p < 0.01), *** ( p < 0.001).

Supportive validation

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Experimental details: Figure 5 Super-resolution images of secretory vesicles in activated platelets. ( a ) 2D STORM images of alpha-granules in the activated platelet. alpha-granules were observed from the platelets that were fixed at different activation time points (0, 5, 10, 15, and 20 min) (yellow arrows: centralization of alpha-granules upon activation). ( b ) The radial distribution graph of alpha-granules showing how alpha-granules-positive pixel density varies as a function of distance from the centroid of the platelet is shown in ( a ), implying the centralization of alpha-granules upon activation. The vacant space in the center was observed at 10-15 min, probably suggesting OCS regions. ( c ) The bar graph indicates the number of alpha-granules per platelet upon activation induced by PMA (mean +- SD; n = 10-23). ( d ) The bar graph indicates the size of alpha-granules upon activation induced by PMA (mean +- SD; n = 19-28). ( e ) The bar graph indicates the averaged alpha-granule-positive pixel number per platelet upon activation induced by PMA (mean +- SD; n = 21). ( f ) 2D STORM images of dense granules in the activated platelet. Dense granules were observed from the platelets that were fixed at different activation time points (0, 5, 10, 15, and 20 min) (yellow arrows: centralization of dense granules upon activation). ( g ) The radial distribution graph of dense granules showing how dense granules-positive pixel density varies as a function of distance from the centroid of the platele

Supportive validation

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Experimental details: Fig. 6 Downregulation of ECM factors in CEBPB -ko cells. a Expression of ECM-associated genes relative to GAPDH in wt BT-20 cells and two different clones of CEBPB -ko BT-20 cells ( n = 3). Results are analysed using one-way ANOVA analysis. Error bars represent SD, ** p < 0.01, **** p < 0.0001. b C/EBPbeta-associated fragments associated with H3K acetylation (H3K27Ac). Data from the ENCODE database ( http://genome.ucsc.edu/ENCODE/ )(see Supplementary Table 1 ). c Immunoblots showing expression of Thrombospondin 1 (THBS1), Tenascin C (TNC), Fibronectin 1 (FN1) or Collagen 5A1 (COL5A1) in wt BT-20 cells and two different clones of Cebpb -ko BT-20 cells. Loss of C/EBPbeta-LAP expression shows the successful CEBPB -knockout and beta-actin was used for loading control.

Supportive validation

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Experimental details: Isolation and characterization of human corneal keratocyte (HCK)-, fibroblast (HCF)-, and myofibroblast (HCM)-derived extracellular vesicles (EVs). ( A ) EV pellets (20 mug protein/lane) were analyzed by western blot to probe for vesicle-associated markers. Representative images are shown for vesicle-associated proteins CD63, CD81, and ITGAV; a negative control (GM130); and proteins associated with corneal wound healing, FN1 and THBS1. ( B ) EV pellets were analyzed by nanoparticle tracking analysis (NTA), and a size distribution histogram for each EV sample is shown. (( B ), inset) Transmission electron microscopy images demonstrating EV morphology (high magnification, 49000x; scale bar = 100 nm). ( C ) The average particle concentrations (particles x1011/mL); ( D ) mean particle size (nm); and ( E ) zeta (zeta) potential of EV pellets were measured using NTA with Zetaview(tm). Data are shown as mean + SEM; n = 3 independent EV preparations; ns = nonsignificant. One-way ANOVA with Tukey's post-test.

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Experimental details: Changes in TSP1 and TSP2 protein expressoin following hemorrhage injury. (A) Representative western blots of TSP1 protein expression and (B) semi-quantification of the band density in the sham group and at each time point after modeling. (C) Representative western blots of TSP2 protein expression and (D) semi-quantification of the band density in the sham group and at each time point after modeling. * P

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Experimental details: 2 The effects of PLK1 downregulation in EC cells. siPLK1 (siPLK286, siPLK785 and siPLK1412) or siNTC was transfected into EC cells. LF- and LF+ represent no transfection and transfection with Lipofectamine RNAiMAX alone, respectively. ( a ) Cell proliferation assay after PLK1-siRNA transfection. HSA/c, KYSE140, KYSE410 and OE33 cells were subjected to WST-8 assay 48 hr after the transfection. The absorbances at 450 nm were measured after 2-hr incubation with WST-8 reagent at 2, 4 and 6 days after plating cells. p values were calculated by two-way ANOVA. ( b ) Cell cycle analysis after PLK1-siRNA transfection. HSA/c and OE33 cells were stained with propidium iodide and analyzed by flow cytometry 48 hr after the siPLK1 transfection. Average percentages of cells in G2/M phase are shown in the representative histograms. ( c ) Localization of PLK1 in siRNA-treated HSA/c cells (magnification x200). HSA/c cells were stained with PLK1, which was labeled with AlexaFluor 568 (red), and nuclei were counterstained with 4',6-diamidine-2'-phenylindole dihydrochloride (DAPI, blue) 48 hr after the siRNA transfection. Left, cells stained with PLK1; middle, cells stained with DAPI; right, merged images. Top, cells transfected with siNTC; bottom, cells transfected with siPLK286. Photographs were taken for identical exposure intervals (70 msec for PLK1 and 3 msec for DAPI). PLK1 was localized mainly to the nuclei of mitotic cells, particularly at the spindle poles from prophase to metaphase (yel

Supportive validation

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Experimental details: Figure 3 High expression of disulphide-HMGB1 in human leukocytes. (A) Western blot probed with anti-CD45, anti-HMGB1, and anti-GAPDH antibodies in reducing conditions (upper panels) or probed with anti-HMGB1 antibody in non-reducing conditions (lower panel) on peripheral blood mononuclear cells (PBMCs) isolated from four healthy human donors. The upper band corresponds to the fully reduced-HMGB1 (frHMGB1) and the lower band to the disulphide-HMGB1 (dsHMGB1) in the lower panel. (B) Quantification of HMGB1 redox isoforms expression normalized on Ponceau staining. A.U. = arbitrary unit ( n = 4 healthy donors). (C,D) Western blot probed with anti-HMGB1 antibody in non-reducing conditions on PBMCs stimulated with anti-CD3/anti-CD28 antibodies or lipopolysaccharide (LPS) for 24 or 72 h (C) . Percentage of HMGB1 redox isoforms expression (D) . Ctrl, control unstimulated cells ( n = 2 healthy donors). Data represent the means +- SEM and statistical significance was calculated by Two-way ANOVA (D) .

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Experimental details: Figure 1 Overexpression of SETDB1 in Melanoma Cell Lines Resulted in the Activation of Protumorigenic-Secreted Factors (A) Histogram plot showing microarray expression data (shown as log 2 fold change) of genes encoding for protumorigenic-secreted factors (THBS1, SCG2, MMP1, MMP3, IL-6, IL-8, CCL2, and WNT5A) in HT 144-SETDB1 OE cells compared to EV cells. (B) Quantitative real-time PCR analysis of the CRS factor-encoding genes SCG2 , MMP3 , IL8 , CCL2 , and WNT5A expression 5. (C) Secretome analysis of HT 144 EV and -SETDB1 OE cell supernatant. Right panel: blots showing the signals of 55 different secreted proteins detected in the supernatant of cultured cells; signals of MMP8 (1), CXCL16 (2), CCL2 (3), and THBS1 (4) are highlighted. Left panel: quantification of mean pixel density related to MMP8, CXCL16, CCL2, and THBS1 signals. Number or replicates: 3. (D) SCG2 immunofluorescence detection in C32 EV (control) and -SCG2 OE cell lines. SCG2-overexpressing cells showed a strong SCG2 signal accumulation at granule structures (indicated by arrows). DAPI stained the nuclei. Scale bars, 20 mum. (E) Tissue microarray analysis (TMA) of a cohort of melanoma patients showing that SETDB1 expression positively correlated with SCG2 expression in melanoma metastases tissue samples. SETDB1 and SCG2 correlation plot is shown. Number of analyzed patients' samples (n), Spearman correlation coefficient (r), and p value are reported. (F) Kaplan-Meier survival analysis of patients with melano