anti av Search Results


92
Proteintech apoa
Mechanical injury and hyperlipidemia induced advanced fatty and lipoproteins deposition beneath the leaflets endothelial. (A) Representative CD31 immunostaining (green, scale bar, 20 μm) and Oil red O staining (top, scale bar, 100 μm; bottom, scale bar, 500 μm) of aortic valves 8 weeks after wire injury. Valvular lipid deposition was only observed in hypercholesterolemic mice 8 weeks after wire injury. (B) Representative images <t>of</t> <t>apoB</t> (scale bar, 50 μm) and <t>apoA</t> (scale bar, 50 μm) lipoproteins in the valvular 8 weeks after wire injury in the indicated groups ( n = 4 per group). (C) Quantification of the valvular lesion area (%) 8 weeks after wire injury in the indicated groups ( n = 4 per group). (D) Quantification of apoB (scale bar, 50 μm) and apoA (scale bar, 50 μm) lipoproteins in the valvular 8 weeks after wire injury in the indicated groups ( n = 4 per group). Results are mean ± SEM. Adjusted P values were provided in case of multiple groups. ns. indicates non-significant P value. ** P < 0.01 and *** P < 0.001.
Apoa, supplied by Proteintech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech apolipoprotein a v apoa5
Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and <t>APOA5</t> proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; <t>APOA5,</t> <t>apolipoprotein</t> <t>A-V;</t> CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
Apolipoprotein A V Apoa5, supplied by Proteintech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+av/pmc10921703-128-66-75?v=Proteintech
Average 92 stars, based on 1 article reviews
apolipoprotein a v apoa5 - by Bioz Stars, 2026-07
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90
Becton Dickinson mouse anti-human av integrin mab
Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and <t>APOA5</t> proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; <t>APOA5,</t> <t>apolipoprotein</t> <t>A-V;</t> CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
Mouse Anti Human Av Integrin Mab, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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BEI Resources mouse monoclonal anti-arenavirus (ow) rgpc, clone kl-av-1b3
Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and <t>APOA5</t> proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; <t>APOA5,</t> <t>apolipoprotein</t> <t>A-V;</t> CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
Mouse Monoclonal Anti Arenavirus (Ow) Rgpc, Clone Kl Av 1b3, supplied by BEI Resources, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse monoclonal anti-arenavirus (ow) rgpc, clone kl-av-1b3 - by Bioz Stars, 2026-07
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90
Becton Dickinson α-gfp rabbit polyclonal
Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and <t>APOA5</t> proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; <t>APOA5,</t> <t>apolipoprotein</t> <t>A-V;</t> CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
α Gfp Rabbit Polyclonal, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Becton Dickinson anti-integrin av 21
Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and <t>APOA5</t> proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; <t>APOA5,</t> <t>apolipoprotein</t> <t>A-V;</t> CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
Anti Integrin Av 21, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Becton Dickinson living colors av peptide (anti-gfp
Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and <t>APOA5</t> proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; <t>APOA5,</t> <t>apolipoprotein</t> <t>A-V;</t> CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
Living Colors Av Peptide (Anti Gfp, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Immunotec inc fitc-conjugated v/cd51 monoclonal antibody clone amf7
Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and <t>APOA5</t> proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; <t>APOA5,</t> <t>apolipoprotein</t> <t>A-V;</t> CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
Fitc Conjugated V/Cd51 Monoclonal Antibody Clone Amf7, supplied by Immunotec inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+av/pm12082459-34-19-27?v=Immunotec+inc
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Medisystems Corporation av fistula needle 17 ga. x 1- 1/4† single pk fw with masterguard anti-stick needle protector
Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and <t>APOA5</t> proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; <t>APOA5,</t> <t>apolipoprotein</t> <t>A-V;</t> CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
Av Fistula Needle 17 Ga. X 1 1/4† Single Pk Fw With Masterguard Anti Stick Needle Protector, supplied by Medisystems Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Medisystems Corporation av fistula needle 17 ga. x 11/4'' single pk fw with masterguard® anti-stick needle protector
Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and <t>APOA5</t> proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; <t>APOA5,</t> <t>apolipoprotein</t> <t>A-V;</t> CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
Av Fistula Needle 17 Ga. X 11/4'' Single Pk Fw With Masterguard® Anti Stick Needle Protector, supplied by Medisystems Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Becton Dickinson r-pe-conjugated anti-mouse antibodies against integrin av integrin a5
Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and <t>APOA5</t> proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; <t>APOA5,</t> <t>apolipoprotein</t> <t>A-V;</t> CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
R Pe Conjugated Anti Mouse Antibodies Against Integrin Av Integrin A5, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Becton Dickinson rat anti-av integrin
Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and <t>APOA5</t> proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; <t>APOA5,</t> <t>apolipoprotein</t> <t>A-V;</t> CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
Rat Anti Av Integrin, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+av/10__7554_slash_elife__22264-193-42-48?v=Becton+Dickinson
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Image Search Results


Mechanical injury and hyperlipidemia induced advanced fatty and lipoproteins deposition beneath the leaflets endothelial. (A) Representative CD31 immunostaining (green, scale bar, 20 μm) and Oil red O staining (top, scale bar, 100 μm; bottom, scale bar, 500 μm) of aortic valves 8 weeks after wire injury. Valvular lipid deposition was only observed in hypercholesterolemic mice 8 weeks after wire injury. (B) Representative images of apoB (scale bar, 50 μm) and apoA (scale bar, 50 μm) lipoproteins in the valvular 8 weeks after wire injury in the indicated groups ( n = 4 per group). (C) Quantification of the valvular lesion area (%) 8 weeks after wire injury in the indicated groups ( n = 4 per group). (D) Quantification of apoB (scale bar, 50 μm) and apoA (scale bar, 50 μm) lipoproteins in the valvular 8 weeks after wire injury in the indicated groups ( n = 4 per group). Results are mean ± SEM. Adjusted P values were provided in case of multiple groups. ns. indicates non-significant P value. ** P < 0.01 and *** P < 0.001.

Journal: Frontiers in Cardiovascular Medicine

Article Title: Mechanical injury accentuates lipid deposition in ApoE –/– mice and advance aortic valve stenosis: A novel modified aortic valve stenosis model

doi: 10.3389/fcvm.2023.1119746

Figure Lengend Snippet: Mechanical injury and hyperlipidemia induced advanced fatty and lipoproteins deposition beneath the leaflets endothelial. (A) Representative CD31 immunostaining (green, scale bar, 20 μm) and Oil red O staining (top, scale bar, 100 μm; bottom, scale bar, 500 μm) of aortic valves 8 weeks after wire injury. Valvular lipid deposition was only observed in hypercholesterolemic mice 8 weeks after wire injury. (B) Representative images of apoB (scale bar, 50 μm) and apoA (scale bar, 50 μm) lipoproteins in the valvular 8 weeks after wire injury in the indicated groups ( n = 4 per group). (C) Quantification of the valvular lesion area (%) 8 weeks after wire injury in the indicated groups ( n = 4 per group). (D) Quantification of apoB (scale bar, 50 μm) and apoA (scale bar, 50 μm) lipoproteins in the valvular 8 weeks after wire injury in the indicated groups ( n = 4 per group). Results are mean ± SEM. Adjusted P values were provided in case of multiple groups. ns. indicates non-significant P value. ** P < 0.01 and *** P < 0.001.

Article Snippet: For immunohistochemistry, sections were incubated with antibodies against apoB (1:50 Proteintech), apoA (1:50 Proteintech), F4/80 (1:50, ab111101, Abcam).

Techniques: Immunostaining, Staining

Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and APOA5 proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5, apolipoprotein A-V; CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)

Journal: Journal of Translational Medicine

Article Title: Characterization of the proteome of stable and unstable carotid atherosclerotic plaques using data-independent acquisition mass spectrometry

doi: 10.1186/s12967-023-04723-1

Figure Lengend Snippet: Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and APOA5 proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5, apolipoprotein A-V; CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)

Article Snippet: Primary antibodies for IHC against solute carrier family 1, member 5 (SLC1A5) (rabbit polyclonal, 20350-1-AP), apoptosis-inducing factor 2 (AIFM2) (rabbit polyclonal, 20886–1-AP), BH3 interacting-domain death agonist (BID) (rabbit polyclonal, 10988-1-AP), dipeptidyl peptidase 4 (DPP4) (rabbit polyclonal, 29403-1-AP), transferrin receptor protein 1 (TFR1) (mouse monoclonal, 66180–1-Ig), transferrin (TF) (rabbit polyclonal, 17435-1-AP), glutamate–cysteine ligase catalytic (GCLC) (rabbit polyclonal, 12601–1-AP), cholesteryl ester transfer protein (CETP) (rabbit polyclonal, 13459-1-AP), and apolipoprotein A-V (APOA5) (rabbit polyclonal, 18019-1-AP) were purchased from Proteintech (China).

Techniques: Biomarker Discovery, Immunohistochemical staining, Staining, Immunohistochemistry, Two Tailed Test

The differently expressed proteins (DEPs) that were validated using immunohistochemistry (all up regulated) (unstable/stable)

Journal: Journal of Translational Medicine

Article Title: Characterization of the proteome of stable and unstable carotid atherosclerotic plaques using data-independent acquisition mass spectrometry

doi: 10.1186/s12967-023-04723-1

Figure Lengend Snippet: The differently expressed proteins (DEPs) that were validated using immunohistochemistry (all up regulated) (unstable/stable)

Article Snippet: Primary antibodies for IHC against solute carrier family 1, member 5 (SLC1A5) (rabbit polyclonal, 20350-1-AP), apoptosis-inducing factor 2 (AIFM2) (rabbit polyclonal, 20886–1-AP), BH3 interacting-domain death agonist (BID) (rabbit polyclonal, 10988-1-AP), dipeptidyl peptidase 4 (DPP4) (rabbit polyclonal, 29403-1-AP), transferrin receptor protein 1 (TFR1) (mouse monoclonal, 66180–1-Ig), transferrin (TF) (rabbit polyclonal, 17435-1-AP), glutamate–cysteine ligase catalytic (GCLC) (rabbit polyclonal, 12601–1-AP), cholesteryl ester transfer protein (CETP) (rabbit polyclonal, 13459-1-AP), and apolipoprotein A-V (APOA5) (rabbit polyclonal, 18019-1-AP) were purchased from Proteintech (China).

Techniques: Immunohistochemistry, Biomarker Discovery, Significance Assay

Hypothetical characterization of altered molecular mechanisms in cells in the fibrous cap and lipid core regions of unstable carotid plaques. The expression of key proteins of ferroptosis and lipid metabolism is significantly increased in patients with unstable plaques, and there are mechanisms associated with both the promotion and inhibition of iron death. This possibly indicates that cells in different regions of the plaque are regulated by key proteins of ferroptosis that subsequently lead to increased plaque instability and expansion of the necrotic core. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic; SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5 apolipoprotein A-V; CETP cholesteryl ester transfer protein; GPX4 glutathione peroxidase 4; GSH glutathione; CoQ10 coenzyme Q10; ROS reactive oxygen species; HDL high-density lipoprotein; ox-LDL oxidized low-density lipoprotein

Journal: Journal of Translational Medicine

Article Title: Characterization of the proteome of stable and unstable carotid atherosclerotic plaques using data-independent acquisition mass spectrometry

doi: 10.1186/s12967-023-04723-1

Figure Lengend Snippet: Hypothetical characterization of altered molecular mechanisms in cells in the fibrous cap and lipid core regions of unstable carotid plaques. The expression of key proteins of ferroptosis and lipid metabolism is significantly increased in patients with unstable plaques, and there are mechanisms associated with both the promotion and inhibition of iron death. This possibly indicates that cells in different regions of the plaque are regulated by key proteins of ferroptosis that subsequently lead to increased plaque instability and expansion of the necrotic core. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic; SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5 apolipoprotein A-V; CETP cholesteryl ester transfer protein; GPX4 glutathione peroxidase 4; GSH glutathione; CoQ10 coenzyme Q10; ROS reactive oxygen species; HDL high-density lipoprotein; ox-LDL oxidized low-density lipoprotein

Article Snippet: Primary antibodies for IHC against solute carrier family 1, member 5 (SLC1A5) (rabbit polyclonal, 20350-1-AP), apoptosis-inducing factor 2 (AIFM2) (rabbit polyclonal, 20886–1-AP), BH3 interacting-domain death agonist (BID) (rabbit polyclonal, 10988-1-AP), dipeptidyl peptidase 4 (DPP4) (rabbit polyclonal, 29403-1-AP), transferrin receptor protein 1 (TFR1) (mouse monoclonal, 66180–1-Ig), transferrin (TF) (rabbit polyclonal, 17435-1-AP), glutamate–cysteine ligase catalytic (GCLC) (rabbit polyclonal, 12601–1-AP), cholesteryl ester transfer protein (CETP) (rabbit polyclonal, 13459-1-AP), and apolipoprotein A-V (APOA5) (rabbit polyclonal, 18019-1-AP) were purchased from Proteintech (China).

Techniques: Expressing, Inhibition