anti jam a bv16 mab  (Hycult Biotech)


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    Hycult Biotech anti jam a bv16 mab
    Anti Jam A Bv16 Mab, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    human jam a fitc conjugated  (Hycult Biotech)


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    Hycult Biotech human jam a fitc conjugated
    HSP does not affect colonic barrier integrity in an ex vivo culture model. Expression of <t>JAM-A</t> (red, (A) ) and E-CAD (green, (B) ) on tissues incubated with three HSP pools for 90 minutes, from 14 HIV infected patients (HIV1-pool), 12 HIV negative fertile subjects (Fertile-pool) or 21 randomly selected donors (Random-pool). Tight junctions were stained with the JAM-A <t>FITC</t> conjugated mAb, and adherent junctions with the E-CAD mAb followed by Alexa Fluor 546-conjugated goat anti-mouse IgG1 antibody. DAPI stained the nuclei (blue). 40X objective magnification are shown.
    Human Jam A Fitc Conjugated, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Human seminal plasma stimulates the migration of CD11c+ mononuclear phagocytes to the apical side of the colonic epithelium without altering the junctional complexes in an ex vivo human intestinal model"

    Article Title: Human seminal plasma stimulates the migration of CD11c+ mononuclear phagocytes to the apical side of the colonic epithelium without altering the junctional complexes in an ex vivo human intestinal model

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2023.1133886

    HSP does not affect colonic barrier integrity in an ex vivo culture model. Expression of JAM-A (red, (A) ) and E-CAD (green, (B) ) on tissues incubated with three HSP pools for 90 minutes, from 14 HIV infected patients (HIV1-pool), 12 HIV negative fertile subjects (Fertile-pool) or 21 randomly selected donors (Random-pool). Tight junctions were stained with the JAM-A FITC conjugated mAb, and adherent junctions with the E-CAD mAb followed by Alexa Fluor 546-conjugated goat anti-mouse IgG1 antibody. DAPI stained the nuclei (blue). 40X objective magnification are shown.
    Figure Legend Snippet: HSP does not affect colonic barrier integrity in an ex vivo culture model. Expression of JAM-A (red, (A) ) and E-CAD (green, (B) ) on tissues incubated with three HSP pools for 90 minutes, from 14 HIV infected patients (HIV1-pool), 12 HIV negative fertile subjects (Fertile-pool) or 21 randomly selected donors (Random-pool). Tight junctions were stained with the JAM-A FITC conjugated mAb, and adherent junctions with the E-CAD mAb followed by Alexa Fluor 546-conjugated goat anti-mouse IgG1 antibody. DAPI stained the nuclei (blue). 40X objective magnification are shown.

    Techniques Used: Ex Vivo, Expressing, Incubation, Infection, Staining

    mouse anti jam a  (Hycult Biotech)


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    Hycult Biotech mouse anti jam a
    Mouse Anti Jam A, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti jam a antibody  (Hycult Biotech)


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    Hycult Biotech anti jam a antibody
    ( A ) HNSCC and dysplasia, ( B ) cancer pearl region, ( C ) invasive region, ( D ) metastatic lymph node. Bar: 100 μm. ( E ) Real-time PCR for mRNAs <t>of</t> <t>JAM-A</t> and β-catenin in tonsil and HNSCC-patient tissues. Results are given as means ± SE. ( F ) ELISA for soluble JAM-A in sera of HNSCC patients and healthy control subjects. Results are given as means ±SE. ( F ) p * < 0.01.
    Anti Jam A Antibody, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Dysregulation of junctional adhesion molecule-A via p63/GATA-3 in head and neck squamous cell carcinoma"

    Article Title: Dysregulation of junctional adhesion molecule-A via p63/GATA-3 in head and neck squamous cell carcinoma

    Journal: Oncotarget

    doi: 10.18632/oncotarget.8432

    ( A ) HNSCC and dysplasia, ( B ) cancer pearl region, ( C ) invasive region, ( D ) metastatic lymph node. Bar: 100 μm. ( E ) Real-time PCR for mRNAs of JAM-A and β-catenin in tonsil and HNSCC-patient tissues. Results are given as means ± SE. ( F ) ELISA for soluble JAM-A in sera of HNSCC patients and healthy control subjects. Results are given as means ±SE. ( F ) p * < 0.01.
    Figure Legend Snippet: ( A ) HNSCC and dysplasia, ( B ) cancer pearl region, ( C ) invasive region, ( D ) metastatic lymph node. Bar: 100 μm. ( E ) Real-time PCR for mRNAs of JAM-A and β-catenin in tonsil and HNSCC-patient tissues. Results are given as means ± SE. ( F ) ELISA for soluble JAM-A in sera of HNSCC patients and healthy control subjects. Results are given as means ±SE. ( F ) p * < 0.01.

    Techniques Used: Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    Proliferation assay ( D ) Matrigel invasion assay ( E ) and images of scratch wound assay ( F ) of Detroit562 cells transfected with negative control siRNA or JAM-A siRNA. Bars: 100 μm. The results are shown as bar graphs. (D, E, F) p * < 0.01.
    Figure Legend Snippet: Proliferation assay ( D ) Matrigel invasion assay ( E ) and images of scratch wound assay ( F ) of Detroit562 cells transfected with negative control siRNA or JAM-A siRNA. Bars: 100 μm. The results are shown as bar graphs. (D, E, F) p * < 0.01.

    Techniques Used: Proliferation Assay, Invasion Assay, Scratch Wound Assay Assay, Transfection, Negative Control

    Western blotting (A) and immunocytochemical staining (B) for JAM-A and β-catenin and flow cytometry (C) for JAM-A in Detroit562 cells treated with the NF-κB inhibitors IMD-0354, MG-132 and curcumin. Bars: 100 μm
    Figure Legend Snippet: Western blotting (A) and immunocytochemical staining (B) for JAM-A and β-catenin and flow cytometry (C) for JAM-A in Detroit562 cells treated with the NF-κB inhibitors IMD-0354, MG-132 and curcumin. Bars: 100 μm

    Techniques Used: Western Blot, Staining, Flow Cytometry

    Bar: 100 μm. Western blotting ( B ) and immunocytochemical staining ( C ) for p63, ΔNp63, JAM-A and β-catenin and flow cytometry ( D ) for JAM-A in Detroit562 cells incubated under hypoxia (2% O 2 ). Bars: 20 μm. ( E ) Real-time PCR for JAM-A mRNA in Detroit562 cells incubated under hypoxia (2% O 2 ). Results are given as means ± SE. p * < 0.01.
    Figure Legend Snippet: Bar: 100 μm. Western blotting ( B ) and immunocytochemical staining ( C ) for p63, ΔNp63, JAM-A and β-catenin and flow cytometry ( D ) for JAM-A in Detroit562 cells incubated under hypoxia (2% O 2 ). Bars: 20 μm. ( E ) Real-time PCR for JAM-A mRNA in Detroit562 cells incubated under hypoxia (2% O 2 ). Results are given as means ± SE. p * < 0.01.

    Techniques Used: Western Blot, Staining, Flow Cytometry, Incubation, Real-time Polymerase Chain Reaction

    ( G ) Flow cytometry for JAM-A in Detroit562 cells transfected with siRNAs of p63, ΔNp63 and GATA-3. Bars: 20 μm.
    Figure Legend Snippet: ( G ) Flow cytometry for JAM-A in Detroit562 cells transfected with siRNAs of p63, ΔNp63 and GATA-3. Bars: 20 μm.

    Techniques Used: Flow Cytometry, Transfection

    ( A ) Images of H.E. and immunocytochemical staining for CK7, p63, ΔNp63, GATA-3, JAM-A and β-catenin in primary cultured cancer cells derived from HNSCC tissue. Bar: 100 μm. Western blotting ( B ) for p63, ΔNp63, GATA-3, JAM-A, β-catenin, occludin and claudin-1, 4, 7 and flow cytometry ( C ) for JAM-A HNSCC in primary cultured cancer cells transfected with siRNAs of p63, ΔNp63, GATA-3 and JAM-A.
    Figure Legend Snippet: ( A ) Images of H.E. and immunocytochemical staining for CK7, p63, ΔNp63, GATA-3, JAM-A and β-catenin in primary cultured cancer cells derived from HNSCC tissue. Bar: 100 μm. Western blotting ( B ) for p63, ΔNp63, GATA-3, JAM-A, β-catenin, occludin and claudin-1, 4, 7 and flow cytometry ( C ) for JAM-A HNSCC in primary cultured cancer cells transfected with siRNAs of p63, ΔNp63, GATA-3 and JAM-A.

    Techniques Used: Staining, Cell Culture, Derivative Assay, Western Blot, Flow Cytometry, Transfection

    anti jam a monoclonal antibody  (Hycult Biotech)


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    Hycult Biotech anti jam a monoclonal antibody
    Anti Jam A Monoclonal Antibody, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti jam a bv16 mab  (Hycult Biotech)


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    Hycult Biotech anti jam a bv16 mab
    Anti Jam A Bv16 Mab, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti jam a bv16 mab  (Hycult Biotech)


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    Hycult Biotech anti jam a bv16 mab
    Anti Jam A Bv16 Mab, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    human jam a  (Hycult Biotech)


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    Hycult Biotech human jam a
    Human Jam A, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti jam a  (Hycult Biotech)


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    Hycult Biotech anti jam a
    Anti Jam A, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti jam a  (Hycult Biotech)


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    Hycult Biotech anti jam a
    Validation of siRNA‐mediated knockdown <t>of</t> <t>JAM‐A</t> in CPC. A, Relative JAM‐A mRNA expression in JAM‐A siRNA–transfected CPC. RNA was collected from the cells 3 days after JAM‐A siRNA transfection (means±SE of duplicate samples). The results shown are representative of those from 3 independent experiments. B, Concentration of soluble JAM‐A in CPC CM. CM was collected from the cells 3 days after JAM‐A siRNA transfection (mean±SEM of duplicate samples). Nontransfected CPCs (−) and CPCs transfected with RNAi negative control were shown as control. CM indicates conditioned medium; CPC, cardiac progenitor cells; JAM‐A, junctional adhesion molecule‐A; siRNA, small interfering RNA.
    Anti Jam A, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti jam a/product/Hycult Biotech
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    anti jam a - by Bioz Stars, 2023-05
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    1) Product Images from "Anti‐Inflammatory Peptides From Cardiac Progenitors Ameliorate Dysfunction After Myocardial Infarction"

    Article Title: Anti‐Inflammatory Peptides From Cardiac Progenitors Ameliorate Dysfunction After Myocardial Infarction

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    doi: 10.1161/JAHA.114.001101

    Validation of siRNA‐mediated knockdown of JAM‐A in CPC. A, Relative JAM‐A mRNA expression in JAM‐A siRNA–transfected CPC. RNA was collected from the cells 3 days after JAM‐A siRNA transfection (means±SE of duplicate samples). The results shown are representative of those from 3 independent experiments. B, Concentration of soluble JAM‐A in CPC CM. CM was collected from the cells 3 days after JAM‐A siRNA transfection (mean±SEM of duplicate samples). Nontransfected CPCs (−) and CPCs transfected with RNAi negative control were shown as control. CM indicates conditioned medium; CPC, cardiac progenitor cells; JAM‐A, junctional adhesion molecule‐A; siRNA, small interfering RNA.
    Figure Legend Snippet: Validation of siRNA‐mediated knockdown of JAM‐A in CPC. A, Relative JAM‐A mRNA expression in JAM‐A siRNA–transfected CPC. RNA was collected from the cells 3 days after JAM‐A siRNA transfection (means±SE of duplicate samples). The results shown are representative of those from 3 independent experiments. B, Concentration of soluble JAM‐A in CPC CM. CM was collected from the cells 3 days after JAM‐A siRNA transfection (mean±SEM of duplicate samples). Nontransfected CPCs (−) and CPCs transfected with RNAi negative control were shown as control. CM indicates conditioned medium; CPC, cardiac progenitor cells; JAM‐A, junctional adhesion molecule‐A; siRNA, small interfering RNA.

    Techniques Used: Expressing, Transfection, Concentration Assay, Negative Control, Small Interfering RNA

    Soluble JAM‐A and CPC CM inhibit transendotherial migration of neutrophils. Neutrophils were pretreated at 37°C for 10 minutes with JAM‐A Fc (10 μg/mL), CPC CM, or CPC CM with anti–JAM‐A antibody (1 μg/mL). Neutrophils were allowed to migrate across HUVECs in response to TNFα (A) or hypoxia‐exposed cardiomyocytes CM (B) for 3 hours. Mean±SEM of 3 experiments. For statistical analysis, 1‐way ANOVA–Tukey–Kramer post hoc test was performed. Significant differences between control and stimulated groups are shown by asterisks (** P <0.01). Additional statistical comparisons are indicated by lines and number signs ( ## P <0.01). CM indicates conditioned medium; CPC, cardiac progenitor cell; HUVEC, human umbilical vein endothelial cell; JAM‐A, junctional adhesion molecule‐A; TNF, tumor necrosis factor.
    Figure Legend Snippet: Soluble JAM‐A and CPC CM inhibit transendotherial migration of neutrophils. Neutrophils were pretreated at 37°C for 10 minutes with JAM‐A Fc (10 μg/mL), CPC CM, or CPC CM with anti–JAM‐A antibody (1 μg/mL). Neutrophils were allowed to migrate across HUVECs in response to TNFα (A) or hypoxia‐exposed cardiomyocytes CM (B) for 3 hours. Mean±SEM of 3 experiments. For statistical analysis, 1‐way ANOVA–Tukey–Kramer post hoc test was performed. Significant differences between control and stimulated groups are shown by asterisks (** P <0.01). Additional statistical comparisons are indicated by lines and number signs ( ## P <0.01). CM indicates conditioned medium; CPC, cardiac progenitor cell; HUVEC, human umbilical vein endothelial cell; JAM‐A, junctional adhesion molecule‐A; TNF, tumor necrosis factor.

    Techniques Used: Migration

    Knockdown of JAM‐A attenuates CPC‐mediated inhibitory effect on neutrophil accumulation. A, Transplantation of CPCs (CPC+PM) but not CPCs transfected with JAM‐A siRNA (JAM‐AsiCPC+PM) reduced relative expression level of Ly6G mRNA. RNA was extracted from left ventricle at 1 day after MI. Expression level was shown as fold changes relative to sham operated mouse using delta delta CT method: sham, n=6; PM, n=7; CPC+PM, n=6; JAM‐AsiCPC+PM, n=5. The Kruskal–Wallis test, followed by the Steel–Dwass test was used for statistical analysis. Asterisks above individual columns indicate significant difference compared with sham. Asterisks above a line spanning 2 columns indicate significant difference between 2 groups (* P <0.05). B, Immunohistochemical images of infarct area stained with anti‐Ly6G and anti‐MPO antibodies at 1 day after MI. Mouse was treated with PM, CPC+PM, or JAM‐AsiCPC+PM. Ly6G and MPO are shown in green and nuclei in blue. Morphology of tissue is shown in nonspecific green fluorescence. Bars were 0.2 mm. C and D, Quantification of neutrophil accumulation in the infarct area of PM‐, CPC+PM–, and JAM‐AsiCPC+PM–treated mice. To obtain the number of Ly6G (C) and that of MPO (D) ‐positive neutrophils/mm 2 in infarct area, 2 heart sections at papillary muscle level were examined per mouse. An average of values obtained from 3 mice for each group was presented. One‐way ANOVA–Tukey–Kramer post hoc test was used for statistical analysis. Asterisks indicate statistical significant differences (** P <0.01 and * P <0.05). CPC indicates cardiac progenitor cell; JAM‐A, junctional adhesion molecule‐A; MI, myocardial infarction; MPO, myeloproxidase; siRNA, small interfering RNA.
    Figure Legend Snippet: Knockdown of JAM‐A attenuates CPC‐mediated inhibitory effect on neutrophil accumulation. A, Transplantation of CPCs (CPC+PM) but not CPCs transfected with JAM‐A siRNA (JAM‐AsiCPC+PM) reduced relative expression level of Ly6G mRNA. RNA was extracted from left ventricle at 1 day after MI. Expression level was shown as fold changes relative to sham operated mouse using delta delta CT method: sham, n=6; PM, n=7; CPC+PM, n=6; JAM‐AsiCPC+PM, n=5. The Kruskal–Wallis test, followed by the Steel–Dwass test was used for statistical analysis. Asterisks above individual columns indicate significant difference compared with sham. Asterisks above a line spanning 2 columns indicate significant difference between 2 groups (* P <0.05). B, Immunohistochemical images of infarct area stained with anti‐Ly6G and anti‐MPO antibodies at 1 day after MI. Mouse was treated with PM, CPC+PM, or JAM‐AsiCPC+PM. Ly6G and MPO are shown in green and nuclei in blue. Morphology of tissue is shown in nonspecific green fluorescence. Bars were 0.2 mm. C and D, Quantification of neutrophil accumulation in the infarct area of PM‐, CPC+PM–, and JAM‐AsiCPC+PM–treated mice. To obtain the number of Ly6G (C) and that of MPO (D) ‐positive neutrophils/mm 2 in infarct area, 2 heart sections at papillary muscle level were examined per mouse. An average of values obtained from 3 mice for each group was presented. One‐way ANOVA–Tukey–Kramer post hoc test was used for statistical analysis. Asterisks indicate statistical significant differences (** P <0.01 and * P <0.05). CPC indicates cardiac progenitor cell; JAM‐A, junctional adhesion molecule‐A; MI, myocardial infarction; MPO, myeloproxidase; siRNA, small interfering RNA.

    Techniques Used: Transplantation Assay, Transfection, Expressing, Immunohistochemical staining, Staining, Fluorescence, Small Interfering RNA

    Injection of JAM‐A Fc protein prevents neutrophil accumulation in ischemic myocardium. A, Transplantation of JAM‐A Fc protein (JAM‐A+PM) reduced relative expression level of Ly6G mRNA. RNA was extracted from left ventricle of day 1 MI heart. Expression level was shown as fold changes relative to sham operated mouse using delta delta CT method: sham, n=4; PM, n=5; JAM‐A+PM, n=5. The Kruskal–Wallis test, followed by the Steel–Dwass test, was used for statistical analysis. Asterisks above individual columns indicate significant difference compared with sham. Asterisks above a line spanning 2 columns indicate significant difference between 2 groups (* P <0.05). B, Immunohistochemical images of infarct area stained with anti‐Ly6G and anti‐MPO antibodies at 1 day after MI. Mouse was treated with PM or JAM‐A+PM. Ly6G and MPO are shown in green and nuclei in blue. Morphology of tissue is shown in nonspecific green fluorescence. Bars were 0.2 mm. C and D, To obtain the number of Ly6G (C) and that of MPO (D) ‐positive neutrophils/mm 2 in infarct area, 2 heart sections at papillary muscle level were examined per mouse. An average of values obtained from 3 mice for each group was presented. Student t test was used for statistical analysis. Asterisks indicate statistical significant differences (** P <0.01 and * P <0.05). JAM‐A, junctional adhesion molecule‐A; MI, myocardial infarction; MPO, myeloproxidase.
    Figure Legend Snippet: Injection of JAM‐A Fc protein prevents neutrophil accumulation in ischemic myocardium. A, Transplantation of JAM‐A Fc protein (JAM‐A+PM) reduced relative expression level of Ly6G mRNA. RNA was extracted from left ventricle of day 1 MI heart. Expression level was shown as fold changes relative to sham operated mouse using delta delta CT method: sham, n=4; PM, n=5; JAM‐A+PM, n=5. The Kruskal–Wallis test, followed by the Steel–Dwass test, was used for statistical analysis. Asterisks above individual columns indicate significant difference compared with sham. Asterisks above a line spanning 2 columns indicate significant difference between 2 groups (* P <0.05). B, Immunohistochemical images of infarct area stained with anti‐Ly6G and anti‐MPO antibodies at 1 day after MI. Mouse was treated with PM or JAM‐A+PM. Ly6G and MPO are shown in green and nuclei in blue. Morphology of tissue is shown in nonspecific green fluorescence. Bars were 0.2 mm. C and D, To obtain the number of Ly6G (C) and that of MPO (D) ‐positive neutrophils/mm 2 in infarct area, 2 heart sections at papillary muscle level were examined per mouse. An average of values obtained from 3 mice for each group was presented. Student t test was used for statistical analysis. Asterisks indicate statistical significant differences (** P <0.01 and * P <0.05). JAM‐A, junctional adhesion molecule‐A; MI, myocardial infarction; MPO, myeloproxidase.

    Techniques Used: Injection, Transplantation Assay, Expressing, Immunohistochemical staining, Staining, Fluorescence

    Injection of JAM‐A+PM attenuates myocardial neutrophil infiltration after MI. Representative dot plots from PM‐ or JAM‐A+PM–treated MI hearts. Cell suspensions from PM‐ or JAM‐A+PM–treated MI hearts were stained with anti–Ly‐6G and anti‐CD45 antibodies. Dot plots from a typical experiment of 2 performed are shown. FITC indicates fluorescein isothiocyanate; JAM‐A, junctional adhesion molecule‐A; MI, myocardial infarction.
    Figure Legend Snippet: Injection of JAM‐A+PM attenuates myocardial neutrophil infiltration after MI. Representative dot plots from PM‐ or JAM‐A+PM–treated MI hearts. Cell suspensions from PM‐ or JAM‐A+PM–treated MI hearts were stained with anti–Ly‐6G and anti‐CD45 antibodies. Dot plots from a typical experiment of 2 performed are shown. FITC indicates fluorescein isothiocyanate; JAM‐A, junctional adhesion molecule‐A; MI, myocardial infarction.

    Techniques Used: Injection, Staining

    Soluble JAM‐A mediates the reduction of infarct size and prevention of left ventricular remodeling, and enhances capillary density. A, Representative Masson's trichrome–stained myocardial sections from PM‐treated, JAM‐A+PM–treated, CPC+PM–treated, and JAM‐AsiCPC+PM–treated hearts. Bars are 2.5 mm. B, Quantification of infarct size 2 weeks after transplantation. For statistical analysis, 1‐way ANOVA–Tukey–Kramer post hoc test was performed. Significant differences among groups are shown by asterisks (** P <0.01 and * P <0.05). C, Representative images from the sections of PM‐treated and JAM‐A+PM–treated hearts stained for capillaries with anti‐vWF antibodies. Bars are 100 μm. D and E, Quantification of the number of vWF‐positive capillaries in border (D) and infarct (E) area 2 weeks after transplantation. To obtain the number of vWF‐positive capillaries/mm 2 in infarct area and border area, 2 heart sections at papillary muscle level were examined per mouse. An average of values obtained from 3 mice for each group was presented. Student t test was used for statistical analysis. Asterisks indicate statistical significant differences (** P <0.01 and * P <0.05). JAM‐A indicates junctional adhesion molecule‐A; vWF, von Willebrand factor.
    Figure Legend Snippet: Soluble JAM‐A mediates the reduction of infarct size and prevention of left ventricular remodeling, and enhances capillary density. A, Representative Masson's trichrome–stained myocardial sections from PM‐treated, JAM‐A+PM–treated, CPC+PM–treated, and JAM‐AsiCPC+PM–treated hearts. Bars are 2.5 mm. B, Quantification of infarct size 2 weeks after transplantation. For statistical analysis, 1‐way ANOVA–Tukey–Kramer post hoc test was performed. Significant differences among groups are shown by asterisks (** P <0.01 and * P <0.05). C, Representative images from the sections of PM‐treated and JAM‐A+PM–treated hearts stained for capillaries with anti‐vWF antibodies. Bars are 100 μm. D and E, Quantification of the number of vWF‐positive capillaries in border (D) and infarct (E) area 2 weeks after transplantation. To obtain the number of vWF‐positive capillaries/mm 2 in infarct area and border area, 2 heart sections at papillary muscle level were examined per mouse. An average of values obtained from 3 mice for each group was presented. Student t test was used for statistical analysis. Asterisks indicate statistical significant differences (** P <0.01 and * P <0.05). JAM‐A indicates junctional adhesion molecule‐A; vWF, von Willebrand factor.

    Techniques Used: Staining, Transplantation Assay

    JAM‐A does not affect scar maturation in infarcted myocardium. A, Representative Picro–Sirius red staining and polarization microscopy in PM‐treated, JAM‐A+PM–treated, CPC+PM–treated, and JAM‐AsiCPC+PM–treated hearts. Bars are 200 μm. B, Quantitative analysis of color component in infarct area. Vertical axis indicates the ratio of pixel number of green to that of yellow‐red. A heart section at the level of the largest scar size was examined per mouse. An average of values obtained from 3 mice for each group was presented. For statistical analysis, 1‐way ANOVA–Tukey–Kramer post hoc test was performed. CPC indicates cardiac progenitor cell; JAM‐A, junctional adhesion molecule‐A.
    Figure Legend Snippet: JAM‐A does not affect scar maturation in infarcted myocardium. A, Representative Picro–Sirius red staining and polarization microscopy in PM‐treated, JAM‐A+PM–treated, CPC+PM–treated, and JAM‐AsiCPC+PM–treated hearts. Bars are 200 μm. B, Quantitative analysis of color component in infarct area. Vertical axis indicates the ratio of pixel number of green to that of yellow‐red. A heart section at the level of the largest scar size was examined per mouse. An average of values obtained from 3 mice for each group was presented. For statistical analysis, 1‐way ANOVA–Tukey–Kramer post hoc test was performed. CPC indicates cardiac progenitor cell; JAM‐A, junctional adhesion molecule‐A.

    Techniques Used: Staining, Microscopy

    Soluble JAM‐A derived from CPC alters the uropod length of neutrophils. A, Actin immunofluorescence staining of neutrophils pretreated with control medium, CPC CM, JAM‐AsiCPC CM, CPC CM+anti‐JAM‐A antibody, or JAM‐A Fc. Bars are 10 μm. B, The frequency of cells with different uropod length in 1 control and 4 treated groups. The graph shows the mean±SEM of 5 experiments. One‐way ANOVA–Tukey–Kramer post hoc test was used for statistical analysis for different uropod length. Asterisks (** P <0.01) indicate significant differences between the treatment and control groups for different uropod length. Number signs ( ## P <0.01) indicate significant differences between the treatment and CPC CM groups for different uropod length. CM indicates conditioned medium; CPC, cardiac progenitor cell; JAM‐A, junctional adhesion molecule‐A.
    Figure Legend Snippet: Soluble JAM‐A derived from CPC alters the uropod length of neutrophils. A, Actin immunofluorescence staining of neutrophils pretreated with control medium, CPC CM, JAM‐AsiCPC CM, CPC CM+anti‐JAM‐A antibody, or JAM‐A Fc. Bars are 10 μm. B, The frequency of cells with different uropod length in 1 control and 4 treated groups. The graph shows the mean±SEM of 5 experiments. One‐way ANOVA–Tukey–Kramer post hoc test was used for statistical analysis for different uropod length. Asterisks (** P <0.01) indicate significant differences between the treatment and control groups for different uropod length. Number signs ( ## P <0.01) indicate significant differences between the treatment and CPC CM groups for different uropod length. CM indicates conditioned medium; CPC, cardiac progenitor cell; JAM‐A, junctional adhesion molecule‐A.

    Techniques Used: Derivative Assay, Immunofluorescence, Staining

    Immunohistochemical images of Sca‐1 and JAM‐A in normal mouse heart. Frozen sections were triple‐stained with Sca‐1 in red, JAM‐A in green, and nuclei in blue. The images overlaid with phase contrast images are shown. White arrowheads indicate perivascular Sca‐1–positive cells, which co‐express JAM‐A. Bars are 50 μm. JAM‐A indicates junctional adhesion molecule‐A.
    Figure Legend Snippet: Immunohistochemical images of Sca‐1 and JAM‐A in normal mouse heart. Frozen sections were triple‐stained with Sca‐1 in red, JAM‐A in green, and nuclei in blue. The images overlaid with phase contrast images are shown. White arrowheads indicate perivascular Sca‐1–positive cells, which co‐express JAM‐A. Bars are 50 μm. JAM‐A indicates junctional adhesion molecule‐A.

    Techniques Used: Immunohistochemical staining, Staining

    Time course of distribution and expression level of JAM‐A following myocardial ischemia. A and B, Frozen sections obtained from border (A) and infarct area (B) 1, 3, 7, and 14 days following MI were stained with CD31 or JAM‐A in red. The samples were costained with smooth muscle actin in green and nuclei in blue. As both CD31 and JAM‐A antibody originated from rat IgG, a pair of serial sections was stained with CD31 and JAM‐A, respectively. White arrowheads indicate CD31 negative nonendothelial JAM‐A–positive cells. Bars are 20 μm. C and D, Semiquantitative immunofluorescence intensity of JAM‐A and CD31 in border (C) and infarct area (D). One mouse was killed at each time point. Two adjacent sections were stained for CD31 and for JAMA separately. The values of immunofluorescence intensity obtained from at least 5 fields were examined. Two main effects and interaction effect were analyzed by using 2‐factor factorial ANOVA (border area [C]; main effect of expressed protein: P =0.27, main effect of time: P =6.5×10 −7 , interaction effect: P =0.75, infarct area [D]; main effect of expressed protein: P =0.0073, main effect of time: P =1.6×10 −9 , interaction effect: P =0.038). The difference in the level of expressed proteins between time points was analyzed by 1‐way ANOVA–Tukey–Kramer post hoc test. Asterisks and number signs above individual columns indicate significant difference compared with day 3 in C and with day 14 in (D) (** P <0.01, * P <0.05, ## P <0.01, and # P <0.05). We performed the experiment twice and similar results were obtained. JAM‐A indicates junctional adhesion molecule‐A; MI, myocardial infarction; SMA, smooth muscle actin.
    Figure Legend Snippet: Time course of distribution and expression level of JAM‐A following myocardial ischemia. A and B, Frozen sections obtained from border (A) and infarct area (B) 1, 3, 7, and 14 days following MI were stained with CD31 or JAM‐A in red. The samples were costained with smooth muscle actin in green and nuclei in blue. As both CD31 and JAM‐A antibody originated from rat IgG, a pair of serial sections was stained with CD31 and JAM‐A, respectively. White arrowheads indicate CD31 negative nonendothelial JAM‐A–positive cells. Bars are 20 μm. C and D, Semiquantitative immunofluorescence intensity of JAM‐A and CD31 in border (C) and infarct area (D). One mouse was killed at each time point. Two adjacent sections were stained for CD31 and for JAMA separately. The values of immunofluorescence intensity obtained from at least 5 fields were examined. Two main effects and interaction effect were analyzed by using 2‐factor factorial ANOVA (border area [C]; main effect of expressed protein: P =0.27, main effect of time: P =6.5×10 −7 , interaction effect: P =0.75, infarct area [D]; main effect of expressed protein: P =0.0073, main effect of time: P =1.6×10 −9 , interaction effect: P =0.038). The difference in the level of expressed proteins between time points was analyzed by 1‐way ANOVA–Tukey–Kramer post hoc test. Asterisks and number signs above individual columns indicate significant difference compared with day 3 in C and with day 14 in (D) (** P <0.01, * P <0.05, ## P <0.01, and # P <0.05). We performed the experiment twice and similar results were obtained. JAM‐A indicates junctional adhesion molecule‐A; MI, myocardial infarction; SMA, smooth muscle actin.

    Techniques Used: Expressing, Staining, Immunofluorescence

    Cardiomyocyte‐like differentiation of transplanted CPCs and proliferation of endogenous CPCs and cardiomyocytes in PM‐ and JAM‐A+PM–treated hearts. A, Representative images of RFP (red) and sarcomeric α‐actinin (green) double‐positive cells (white arrowheads) in epicardial region (upper panels) and border area (lower panels). Nuclei were stained in blue. Bars are 10 μm. B, Number of RFP and sarcomeric α‐actinin double‐positive cells per section of PM‐ and JAM‐A+PM–treated hearts. An average of values obtained from 3 sections per mouse was analyzed: n=3 mice for PM‐ and n=4 mice for JAM‐A+PM–treated group. Student t test was used for statistical analysis. C, Confocal images of BrdU‐positive CPC (white arrowheads) and BrdU‐positive cardiomyocytes (white arrows). Bars are 20 μm. D, Frequency of BrdU‐positive CPCs in total CPCs in PM‐ and JAM‐A+PM–treated hearts. The whole area of LV in a section through the long axis of the heart was examined per mouse: n=3 mice for PM‐ and n=4 mice for JAM‐A+PM–treated group. Student t test was used for statistical analysis. E, Frequency of BrdU‐positive cardiomyocytes in PM‐ and JAM‐A+PM–treated hearts. The whole area of LV in a section through the long axis of the heart was examined per mouse” n=3 mice per group. Student t test was used for statistical analysis. CPC indicates cardiac progenitor cell; JAM‐A, junctional adhesion molecule‐A; LV, left ventricle; RFP, red fluorescent protein.
    Figure Legend Snippet: Cardiomyocyte‐like differentiation of transplanted CPCs and proliferation of endogenous CPCs and cardiomyocytes in PM‐ and JAM‐A+PM–treated hearts. A, Representative images of RFP (red) and sarcomeric α‐actinin (green) double‐positive cells (white arrowheads) in epicardial region (upper panels) and border area (lower panels). Nuclei were stained in blue. Bars are 10 μm. B, Number of RFP and sarcomeric α‐actinin double‐positive cells per section of PM‐ and JAM‐A+PM–treated hearts. An average of values obtained from 3 sections per mouse was analyzed: n=3 mice for PM‐ and n=4 mice for JAM‐A+PM–treated group. Student t test was used for statistical analysis. C, Confocal images of BrdU‐positive CPC (white arrowheads) and BrdU‐positive cardiomyocytes (white arrows). Bars are 20 μm. D, Frequency of BrdU‐positive CPCs in total CPCs in PM‐ and JAM‐A+PM–treated hearts. The whole area of LV in a section through the long axis of the heart was examined per mouse: n=3 mice for PM‐ and n=4 mice for JAM‐A+PM–treated group. Student t test was used for statistical analysis. E, Frequency of BrdU‐positive cardiomyocytes in PM‐ and JAM‐A+PM–treated hearts. The whole area of LV in a section through the long axis of the heart was examined per mouse” n=3 mice per group. Student t test was used for statistical analysis. CPC indicates cardiac progenitor cell; JAM‐A, junctional adhesion molecule‐A; LV, left ventricle; RFP, red fluorescent protein.

    Techniques Used: Staining

    anti jam a antibody  (Hycult Biotech)


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    Hycult Biotech anti jam a antibody
    Anti Jam A Antibody, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Hycult Biotech anti jam a bv16 mab
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    HSP does not affect colonic barrier integrity in an ex vivo culture model. Expression of <t>JAM-A</t> (red, (A) ) and E-CAD (green, (B) ) on tissues incubated with three HSP pools for 90 minutes, from 14 HIV infected patients (HIV1-pool), 12 HIV negative fertile subjects (Fertile-pool) or 21 randomly selected donors (Random-pool). Tight junctions were stained with the JAM-A <t>FITC</t> conjugated mAb, and adherent junctions with the E-CAD mAb followed by Alexa Fluor 546-conjugated goat anti-mouse IgG1 antibody. DAPI stained the nuclei (blue). 40X objective magnification are shown.
    Human Jam A Fitc Conjugated, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    HSP does not affect colonic barrier integrity in an ex vivo culture model. Expression of <t>JAM-A</t> (red, (A) ) and E-CAD (green, (B) ) on tissues incubated with three HSP pools for 90 minutes, from 14 HIV infected patients (HIV1-pool), 12 HIV negative fertile subjects (Fertile-pool) or 21 randomly selected donors (Random-pool). Tight junctions were stained with the JAM-A <t>FITC</t> conjugated mAb, and adherent junctions with the E-CAD mAb followed by Alexa Fluor 546-conjugated goat anti-mouse IgG1 antibody. DAPI stained the nuclei (blue). 40X objective magnification are shown.
    Mouse Anti Jam A, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ( A ) HNSCC and dysplasia, ( B ) cancer pearl region, ( C ) invasive region, ( D ) metastatic lymph node. Bar: 100 μm. ( E ) Real-time PCR for mRNAs <t>of</t> <t>JAM-A</t> and β-catenin in tonsil and HNSCC-patient tissues. Results are given as means ± SE. ( F ) ELISA for soluble JAM-A in sera of HNSCC patients and healthy control subjects. Results are given as means ±SE. ( F ) p * < 0.01.
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    ( A ) HNSCC and dysplasia, ( B ) cancer pearl region, ( C ) invasive region, ( D ) metastatic lymph node. Bar: 100 μm. ( E ) Real-time PCR for mRNAs <t>of</t> <t>JAM-A</t> and β-catenin in tonsil and HNSCC-patient tissues. Results are given as means ± SE. ( F ) ELISA for soluble JAM-A in sera of HNSCC patients and healthy control subjects. Results are given as means ±SE. ( F ) p * < 0.01.
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    ( A ) HNSCC and dysplasia, ( B ) cancer pearl region, ( C ) invasive region, ( D ) metastatic lymph node. Bar: 100 μm. ( E ) Real-time PCR for mRNAs <t>of</t> <t>JAM-A</t> and β-catenin in tonsil and HNSCC-patient tissues. Results are given as means ± SE. ( F ) ELISA for soluble JAM-A in sera of HNSCC patients and healthy control subjects. Results are given as means ±SE. ( F ) p * < 0.01.
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    ( A ) HNSCC and dysplasia, ( B ) cancer pearl region, ( C ) invasive region, ( D ) metastatic lymph node. Bar: 100 μm. ( E ) Real-time PCR for mRNAs <t>of</t> <t>JAM-A</t> and β-catenin in tonsil and HNSCC-patient tissues. Results are given as means ± SE. ( F ) ELISA for soluble JAM-A in sera of HNSCC patients and healthy control subjects. Results are given as means ±SE. ( F ) p * < 0.01.
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    Image Search Results


    HSP does not affect colonic barrier integrity in an ex vivo culture model. Expression of JAM-A (red, (A) ) and E-CAD (green, (B) ) on tissues incubated with three HSP pools for 90 minutes, from 14 HIV infected patients (HIV1-pool), 12 HIV negative fertile subjects (Fertile-pool) or 21 randomly selected donors (Random-pool). Tight junctions were stained with the JAM-A FITC conjugated mAb, and adherent junctions with the E-CAD mAb followed by Alexa Fluor 546-conjugated goat anti-mouse IgG1 antibody. DAPI stained the nuclei (blue). 40X objective magnification are shown.

    Journal: Frontiers in Immunology

    Article Title: Human seminal plasma stimulates the migration of CD11c+ mononuclear phagocytes to the apical side of the colonic epithelium without altering the junctional complexes in an ex vivo human intestinal model

    doi: 10.3389/fimmu.2023.1133886

    Figure Lengend Snippet: HSP does not affect colonic barrier integrity in an ex vivo culture model. Expression of JAM-A (red, (A) ) and E-CAD (green, (B) ) on tissues incubated with three HSP pools for 90 minutes, from 14 HIV infected patients (HIV1-pool), 12 HIV negative fertile subjects (Fertile-pool) or 21 randomly selected donors (Random-pool). Tight junctions were stained with the JAM-A FITC conjugated mAb, and adherent junctions with the E-CAD mAb followed by Alexa Fluor 546-conjugated goat anti-mouse IgG1 antibody. DAPI stained the nuclei (blue). 40X objective magnification are shown.

    Article Snippet: The primary antibody used were: mouse anti human JAM-A FITC conjugated (clone BV16, Hycult biotech, Uden, NL), mouse anti human E-Cadherin (clone 36/E, BD Bioscience, Franklin Lake, NJ, USA), rabbit anti human CD11c (ab52632, ABCAM, Cambridge, UK), and mouse anti human CD64 (ab140779, ABCAM, Cambridge, UK).

    Techniques: Ex Vivo, Expressing, Incubation, Infection, Staining

    ( A ) HNSCC and dysplasia, ( B ) cancer pearl region, ( C ) invasive region, ( D ) metastatic lymph node. Bar: 100 μm. ( E ) Real-time PCR for mRNAs of JAM-A and β-catenin in tonsil and HNSCC-patient tissues. Results are given as means ± SE. ( F ) ELISA for soluble JAM-A in sera of HNSCC patients and healthy control subjects. Results are given as means ±SE. ( F ) p * < 0.01.

    Journal: Oncotarget

    Article Title: Dysregulation of junctional adhesion molecule-A via p63/GATA-3 in head and neck squamous cell carcinoma

    doi: 10.18632/oncotarget.8432

    Figure Lengend Snippet: ( A ) HNSCC and dysplasia, ( B ) cancer pearl region, ( C ) invasive region, ( D ) metastatic lymph node. Bar: 100 μm. ( E ) Real-time PCR for mRNAs of JAM-A and β-catenin in tonsil and HNSCC-patient tissues. Results are given as means ± SE. ( F ) ELISA for soluble JAM-A in sera of HNSCC patients and healthy control subjects. Results are given as means ±SE. ( F ) p * < 0.01.

    Article Snippet: An FITC-conjugated anti-JAM-A antibody was obtained from Hycult biotech (Plymouth Meeting, PA).

    Techniques: Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    Proliferation assay ( D ) Matrigel invasion assay ( E ) and images of scratch wound assay ( F ) of Detroit562 cells transfected with negative control siRNA or JAM-A siRNA. Bars: 100 μm. The results are shown as bar graphs. (D, E, F) p * < 0.01.

    Journal: Oncotarget

    Article Title: Dysregulation of junctional adhesion molecule-A via p63/GATA-3 in head and neck squamous cell carcinoma

    doi: 10.18632/oncotarget.8432

    Figure Lengend Snippet: Proliferation assay ( D ) Matrigel invasion assay ( E ) and images of scratch wound assay ( F ) of Detroit562 cells transfected with negative control siRNA or JAM-A siRNA. Bars: 100 μm. The results are shown as bar graphs. (D, E, F) p * < 0.01.

    Article Snippet: An FITC-conjugated anti-JAM-A antibody was obtained from Hycult biotech (Plymouth Meeting, PA).

    Techniques: Proliferation Assay, Invasion Assay, Scratch Wound Assay Assay, Transfection, Negative Control

    Western blotting (A) and immunocytochemical staining (B) for JAM-A and β-catenin and flow cytometry (C) for JAM-A in Detroit562 cells treated with the NF-κB inhibitors IMD-0354, MG-132 and curcumin. Bars: 100 μm

    Journal: Oncotarget

    Article Title: Dysregulation of junctional adhesion molecule-A via p63/GATA-3 in head and neck squamous cell carcinoma

    doi: 10.18632/oncotarget.8432

    Figure Lengend Snippet: Western blotting (A) and immunocytochemical staining (B) for JAM-A and β-catenin and flow cytometry (C) for JAM-A in Detroit562 cells treated with the NF-κB inhibitors IMD-0354, MG-132 and curcumin. Bars: 100 μm

    Article Snippet: An FITC-conjugated anti-JAM-A antibody was obtained from Hycult biotech (Plymouth Meeting, PA).

    Techniques: Western Blot, Staining, Flow Cytometry

    Bar: 100 μm. Western blotting ( B ) and immunocytochemical staining ( C ) for p63, ΔNp63, JAM-A and β-catenin and flow cytometry ( D ) for JAM-A in Detroit562 cells incubated under hypoxia (2% O 2 ). Bars: 20 μm. ( E ) Real-time PCR for JAM-A mRNA in Detroit562 cells incubated under hypoxia (2% O 2 ). Results are given as means ± SE. p * < 0.01.

    Journal: Oncotarget

    Article Title: Dysregulation of junctional adhesion molecule-A via p63/GATA-3 in head and neck squamous cell carcinoma

    doi: 10.18632/oncotarget.8432

    Figure Lengend Snippet: Bar: 100 μm. Western blotting ( B ) and immunocytochemical staining ( C ) for p63, ΔNp63, JAM-A and β-catenin and flow cytometry ( D ) for JAM-A in Detroit562 cells incubated under hypoxia (2% O 2 ). Bars: 20 μm. ( E ) Real-time PCR for JAM-A mRNA in Detroit562 cells incubated under hypoxia (2% O 2 ). Results are given as means ± SE. p * < 0.01.

    Article Snippet: An FITC-conjugated anti-JAM-A antibody was obtained from Hycult biotech (Plymouth Meeting, PA).

    Techniques: Western Blot, Staining, Flow Cytometry, Incubation, Real-time Polymerase Chain Reaction

    ( G ) Flow cytometry for JAM-A in Detroit562 cells transfected with siRNAs of p63, ΔNp63 and GATA-3. Bars: 20 μm.

    Journal: Oncotarget

    Article Title: Dysregulation of junctional adhesion molecule-A via p63/GATA-3 in head and neck squamous cell carcinoma

    doi: 10.18632/oncotarget.8432

    Figure Lengend Snippet: ( G ) Flow cytometry for JAM-A in Detroit562 cells transfected with siRNAs of p63, ΔNp63 and GATA-3. Bars: 20 μm.

    Article Snippet: An FITC-conjugated anti-JAM-A antibody was obtained from Hycult biotech (Plymouth Meeting, PA).

    Techniques: Flow Cytometry, Transfection

    ( A ) Images of H.E. and immunocytochemical staining for CK7, p63, ΔNp63, GATA-3, JAM-A and β-catenin in primary cultured cancer cells derived from HNSCC tissue. Bar: 100 μm. Western blotting ( B ) for p63, ΔNp63, GATA-3, JAM-A, β-catenin, occludin and claudin-1, 4, 7 and flow cytometry ( C ) for JAM-A HNSCC in primary cultured cancer cells transfected with siRNAs of p63, ΔNp63, GATA-3 and JAM-A.

    Journal: Oncotarget

    Article Title: Dysregulation of junctional adhesion molecule-A via p63/GATA-3 in head and neck squamous cell carcinoma

    doi: 10.18632/oncotarget.8432

    Figure Lengend Snippet: ( A ) Images of H.E. and immunocytochemical staining for CK7, p63, ΔNp63, GATA-3, JAM-A and β-catenin in primary cultured cancer cells derived from HNSCC tissue. Bar: 100 μm. Western blotting ( B ) for p63, ΔNp63, GATA-3, JAM-A, β-catenin, occludin and claudin-1, 4, 7 and flow cytometry ( C ) for JAM-A HNSCC in primary cultured cancer cells transfected with siRNAs of p63, ΔNp63, GATA-3 and JAM-A.

    Article Snippet: An FITC-conjugated anti-JAM-A antibody was obtained from Hycult biotech (Plymouth Meeting, PA).

    Techniques: Staining, Cell Culture, Derivative Assay, Western Blot, Flow Cytometry, Transfection