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4◦cwith primary antibodies against cd31  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc 4◦cwith primary antibodies against cd31
    FIGURE 1 Cerebral vessels lesion and elevated <t>CD31</t> levels related to tau pathology in human AD brains. Representative western blots of the level of CD31 (endothelial marker), αSMA (smooth muscle marker), and PDGFRβ (pericyte marker) in separated cerebral vessels of human non-ADD (n = 9) and AD brains (n = 20). Relative expression of αSMA and PDGFRβ normalized to CD31. (A) While both αSMA/CD31 and PDGFRβ/CD31 in cerebral vessels were reduced in human AD brains compared to non-AD brains, CD31 levels showed no difference between the two groups. (B) Schematic of extraction of soluble (TBS fraction), membrane (TBSX fraction) and insoluble proteins (GuHCl fraction) from frozen human brains by a three–step ultracentrifugation. (C) Quantification of occludin, Claudin-5, and CD31 in TBSX fraction by ELISA. Both occludin/CD31 and Claudin-5/CD31 were reduced in human AD brains (n = 7) compared to non-ADD brains (n = 24). (D) Quantification of Aβ42, Aβ40 and pTau181 in GuHCl fraction by MSD. The high pathological group is defined as having levels of Aβ42, Aβ40, or pTau181 greater than the median of the AD group. (E) Univariate or multivariate analyses was used to test associations between Aβ42, Aβ40, pTau181 in GuHCl fraction and CD31 in TBSX fraction with age, sex, and APOE genotype as covariates. Group differences were assessed using ANCOVA adjusted age, sex, and APOE genotype, following by Bonferroni multiple comparison tests. *p < 0.05, **p < 0.01. AD, Alzheimer’s disease; ANCOVA, analysis of covariance; APOE, apolipoprotein E.
    4◦Cwith Primary Antibodies Against Cd31, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 727 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/4%E2%97%A6cwith+primary+antibodies+against+cd31/CD31+(PECAM-1)+Mouse+mAb/pm39777972-63-30-35
    Average 96 stars, based on 727 article reviews
    4◦cwith primary antibodies against cd31 - by Bioz Stars, 2026-09
    96/100 stars

    Images

    1) Product Images from "Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease."

    Article Title: Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease.

    Journal: Alzheimer's & dementia : the journal of the Alzheimer's Association

    doi: 10.1002/alz.14521

    FIGURE 1 Cerebral vessels lesion and elevated CD31 levels related to tau pathology in human AD brains. Representative western blots of the level of CD31 (endothelial marker), αSMA (smooth muscle marker), and PDGFRβ (pericyte marker) in separated cerebral vessels of human non-ADD (n = 9) and AD brains (n = 20). Relative expression of αSMA and PDGFRβ normalized to CD31. (A) While both αSMA/CD31 and PDGFRβ/CD31 in cerebral vessels were reduced in human AD brains compared to non-AD brains, CD31 levels showed no difference between the two groups. (B) Schematic of extraction of soluble (TBS fraction), membrane (TBSX fraction) and insoluble proteins (GuHCl fraction) from frozen human brains by a three–step ultracentrifugation. (C) Quantification of occludin, Claudin-5, and CD31 in TBSX fraction by ELISA. Both occludin/CD31 and Claudin-5/CD31 were reduced in human AD brains (n = 7) compared to non-ADD brains (n = 24). (D) Quantification of Aβ42, Aβ40 and pTau181 in GuHCl fraction by MSD. The high pathological group is defined as having levels of Aβ42, Aβ40, or pTau181 greater than the median of the AD group. (E) Univariate or multivariate analyses was used to test associations between Aβ42, Aβ40, pTau181 in GuHCl fraction and CD31 in TBSX fraction with age, sex, and APOE genotype as covariates. Group differences were assessed using ANCOVA adjusted age, sex, and APOE genotype, following by Bonferroni multiple comparison tests. *p < 0.05, **p < 0.01. AD, Alzheimer’s disease; ANCOVA, analysis of covariance; APOE, apolipoprotein E.
    Figure Legend Snippet: FIGURE 1 Cerebral vessels lesion and elevated CD31 levels related to tau pathology in human AD brains. Representative western blots of the level of CD31 (endothelial marker), αSMA (smooth muscle marker), and PDGFRβ (pericyte marker) in separated cerebral vessels of human non-ADD (n = 9) and AD brains (n = 20). Relative expression of αSMA and PDGFRβ normalized to CD31. (A) While both αSMA/CD31 and PDGFRβ/CD31 in cerebral vessels were reduced in human AD brains compared to non-AD brains, CD31 levels showed no difference between the two groups. (B) Schematic of extraction of soluble (TBS fraction), membrane (TBSX fraction) and insoluble proteins (GuHCl fraction) from frozen human brains by a three–step ultracentrifugation. (C) Quantification of occludin, Claudin-5, and CD31 in TBSX fraction by ELISA. Both occludin/CD31 and Claudin-5/CD31 were reduced in human AD brains (n = 7) compared to non-ADD brains (n = 24). (D) Quantification of Aβ42, Aβ40 and pTau181 in GuHCl fraction by MSD. The high pathological group is defined as having levels of Aβ42, Aβ40, or pTau181 greater than the median of the AD group. (E) Univariate or multivariate analyses was used to test associations between Aβ42, Aβ40, pTau181 in GuHCl fraction and CD31 in TBSX fraction with age, sex, and APOE genotype as covariates. Group differences were assessed using ANCOVA adjusted age, sex, and APOE genotype, following by Bonferroni multiple comparison tests. *p < 0.05, **p < 0.01. AD, Alzheimer’s disease; ANCOVA, analysis of covariance; APOE, apolipoprotein E.

    Techniques Used: Western Blot, Marker, Expressing, Extraction, Membrane, Enzyme-linked Immunosorbent Assay, Comparison

    Related Articles

    Blocking Assay:

    Article Title: Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease.
    Article Snippet: .. The sections were then blocked with blocking buffer (5% normal goat serum, 0.3% Triton ×-100 in phosphate buffered saline [PBS]) for 1 h at room temperature and incubated overnight at 4◦Cwith primary antibodies against CD31 (CST, 3528S, 1:200) and CD13 (Proteintech, 66211-1-Ig, 1:200). .. After washing with PBST (0.05% Tween-20 in PBS), sections were incubated with Goat anti-Mouse Alexa Fluor 647 (CST, 4410, 1:500) for 1.5 h at room temperature, followed by incubation with DAPI.

    Saline:

    Article Title: Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease.
    Article Snippet: .. The sections were then blocked with blocking buffer (5% normal goat serum, 0.3% Triton ×-100 in phosphate buffered saline [PBS]) for 1 h at room temperature and incubated overnight at 4◦Cwith primary antibodies against CD31 (CST, 3528S, 1:200) and CD13 (Proteintech, 66211-1-Ig, 1:200). .. After washing with PBST (0.05% Tween-20 in PBS), sections were incubated with Goat anti-Mouse Alexa Fluor 647 (CST, 4410, 1:500) for 1.5 h at room temperature, followed by incubation with DAPI.

    Incubation:

    Article Title: Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease.
    Article Snippet: .. The sections were then blocked with blocking buffer (5% normal goat serum, 0.3% Triton ×-100 in phosphate buffered saline [PBS]) for 1 h at room temperature and incubated overnight at 4◦Cwith primary antibodies against CD31 (CST, 3528S, 1:200) and CD13 (Proteintech, 66211-1-Ig, 1:200). .. After washing with PBST (0.05% Tween-20 in PBS), sections were incubated with Goat anti-Mouse Alexa Fluor 647 (CST, 4410, 1:500) for 1.5 h at room temperature, followed by incubation with DAPI.



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    4◦cwith primary antibodies against cd31  (Cell Signaling Technology Inc)
    96
    Cell Signaling Technology Inc 4◦cwith primary antibodies against cd31
    FIGURE 1 Cerebral vessels lesion and elevated <t>CD31</t> levels related to tau pathology in human AD brains. Representative western blots of the level of CD31 (endothelial marker), αSMA (smooth muscle marker), and PDGFRβ (pericyte marker) in separated cerebral vessels of human non-ADD (n = 9) and AD brains (n = 20). Relative expression of αSMA and PDGFRβ normalized to CD31. (A) While both αSMA/CD31 and PDGFRβ/CD31 in cerebral vessels were reduced in human AD brains compared to non-AD brains, CD31 levels showed no difference between the two groups. (B) Schematic of extraction of soluble (TBS fraction), membrane (TBSX fraction) and insoluble proteins (GuHCl fraction) from frozen human brains by a three–step ultracentrifugation. (C) Quantification of occludin, Claudin-5, and CD31 in TBSX fraction by ELISA. Both occludin/CD31 and Claudin-5/CD31 were reduced in human AD brains (n = 7) compared to non-ADD brains (n = 24). (D) Quantification of Aβ42, Aβ40 and pTau181 in GuHCl fraction by MSD. The high pathological group is defined as having levels of Aβ42, Aβ40, or pTau181 greater than the median of the AD group. (E) Univariate or multivariate analyses was used to test associations between Aβ42, Aβ40, pTau181 in GuHCl fraction and CD31 in TBSX fraction with age, sex, and APOE genotype as covariates. Group differences were assessed using ANCOVA adjusted age, sex, and APOE genotype, following by Bonferroni multiple comparison tests. *p < 0.05, **p < 0.01. AD, Alzheimer’s disease; ANCOVA, analysis of covariance; APOE, apolipoprotein E.
    4◦Cwith Primary Antibodies Against Cd31, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/4%E2%97%A6cwith+primary+antibodies+against+cd31/CD31+(PECAM-1)+Mouse+mAb/pm39777972-63-30-35
    Average 96 stars, based on 1 article reviews
    4◦cwith primary antibodies against cd31 - by Bioz Stars, 2026-09
    96/100 stars
    		  Buy from Supplier

    Image Search Results


    FIGURE 1 Cerebral vessels lesion and elevated CD31 levels related to tau pathology in human AD brains. Representative western blots of the level of CD31 (endothelial marker), αSMA (smooth muscle marker), and PDGFRβ (pericyte marker) in separated cerebral vessels of human non-ADD (n = 9) and AD brains (n = 20). Relative expression of αSMA and PDGFRβ normalized to CD31. (A) While both αSMA/CD31 and PDGFRβ/CD31 in cerebral vessels were reduced in human AD brains compared to non-AD brains, CD31 levels showed no difference between the two groups. (B) Schematic of extraction of soluble (TBS fraction), membrane (TBSX fraction) and insoluble proteins (GuHCl fraction) from frozen human brains by a three–step ultracentrifugation. (C) Quantification of occludin, Claudin-5, and CD31 in TBSX fraction by ELISA. Both occludin/CD31 and Claudin-5/CD31 were reduced in human AD brains (n = 7) compared to non-ADD brains (n = 24). (D) Quantification of Aβ42, Aβ40 and pTau181 in GuHCl fraction by MSD. The high pathological group is defined as having levels of Aβ42, Aβ40, or pTau181 greater than the median of the AD group. (E) Univariate or multivariate analyses was used to test associations between Aβ42, Aβ40, pTau181 in GuHCl fraction and CD31 in TBSX fraction with age, sex, and APOE genotype as covariates. Group differences were assessed using ANCOVA adjusted age, sex, and APOE genotype, following by Bonferroni multiple comparison tests. *p < 0.05, **p < 0.01. AD, Alzheimer’s disease; ANCOVA, analysis of covariance; APOE, apolipoprotein E.

    Journal: Alzheimer's & dementia : the journal of the Alzheimer's Association

    Article Title: Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease.

    doi: 10.1002/alz.14521

    Figure Lengend Snippet: FIGURE 1 Cerebral vessels lesion and elevated CD31 levels related to tau pathology in human AD brains. Representative western blots of the level of CD31 (endothelial marker), αSMA (smooth muscle marker), and PDGFRβ (pericyte marker) in separated cerebral vessels of human non-ADD (n = 9) and AD brains (n = 20). Relative expression of αSMA and PDGFRβ normalized to CD31. (A) While both αSMA/CD31 and PDGFRβ/CD31 in cerebral vessels were reduced in human AD brains compared to non-AD brains, CD31 levels showed no difference between the two groups. (B) Schematic of extraction of soluble (TBS fraction), membrane (TBSX fraction) and insoluble proteins (GuHCl fraction) from frozen human brains by a three–step ultracentrifugation. (C) Quantification of occludin, Claudin-5, and CD31 in TBSX fraction by ELISA. Both occludin/CD31 and Claudin-5/CD31 were reduced in human AD brains (n = 7) compared to non-ADD brains (n = 24). (D) Quantification of Aβ42, Aβ40 and pTau181 in GuHCl fraction by MSD. The high pathological group is defined as having levels of Aβ42, Aβ40, or pTau181 greater than the median of the AD group. (E) Univariate or multivariate analyses was used to test associations between Aβ42, Aβ40, pTau181 in GuHCl fraction and CD31 in TBSX fraction with age, sex, and APOE genotype as covariates. Group differences were assessed using ANCOVA adjusted age, sex, and APOE genotype, following by Bonferroni multiple comparison tests. *p < 0.05, **p < 0.01. AD, Alzheimer’s disease; ANCOVA, analysis of covariance; APOE, apolipoprotein E.

    Article Snippet: The sections were then blocked with blocking buffer (5% normal goat serum, 0.3% Triton ×-100 in phosphate buffered saline [PBS]) for 1 h at room temperature and incubated overnight at 4◦Cwith primary antibodies against CD31 (CST, 3528S, 1:200) and CD13 (Proteintech, 66211-1-Ig, 1:200).

    Techniques: Western Blot, Marker, Expressing, Extraction, Membrane, Enzyme-linked Immunosorbent Assay, Comparison