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antibodies against abcb1  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc antibodies against abcb1
    Antibodies Against Abcb1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 475 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against abcb1/product/Cell Signaling Technology Inc
    Average 96 stars, based on 475 article reviews
    antibodies against abcb1 - by Bioz Stars, 2026-05
    96/100 stars

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    Effects of Que on cell viability, mRNA levels, apoptosis and protein expression in MCF-7 cells. (A) Cell viability of MCF-7 cells treated with the indicated concentrations of Que for 24 and 48 h, as determined by the Cell Cycle Kit-8 assay. (B) mRNA expression levels of <t>ABCB1,</t> ABCC2 and ABCG2 following Que treatment. (C) Representative western blotting images, (D) protein expression levels of ABCB1, ABCC2 and ABCG2, and (E) Bax, Bcl-2, and cleaved caspase-3 were assessed by western blotting. (F) Representative images of flow cytometry and (G) apoptosis rate was analyzed by flow cytometry after Annexin V-FITC/PI staining. Data are presented as the mean ± SEM of at least three independent experiments. Statistical significance was determined by one/two-way ANOVA followed by Bonferroni's post hoc test for multiple comparisons. *P<0.05, **P<0.01 compared with the control group, ## P<0.01 compared with the Que (24 h) group. Que, Quercetin; Ctrl, control.
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    Effects of Que on cell viability, mRNA levels, apoptosis and protein expression in MCF-7 cells. (A) Cell viability of MCF-7 cells treated with the indicated concentrations of Que for 24 and 48 h, as determined by the Cell Cycle Kit-8 assay. (B) mRNA expression levels of <t>ABCB1,</t> ABCC2 and ABCG2 following Que treatment. (C) Representative western blotting images, (D) protein expression levels of ABCB1, ABCC2 and ABCG2, and (E) Bax, Bcl-2, and cleaved caspase-3 were assessed by western blotting. (F) Representative images of flow cytometry and (G) apoptosis rate was analyzed by flow cytometry after Annexin V-FITC/PI staining. Data are presented as the mean ± SEM of at least three independent experiments. Statistical significance was determined by one/two-way ANOVA followed by Bonferroni's post hoc test for multiple comparisons. *P<0.05, **P<0.01 compared with the control group, ## P<0.01 compared with the Que (24 h) group. Que, Quercetin; Ctrl, control.
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    Effects of Que on cell viability, mRNA levels, apoptosis and protein expression in MCF-7 cells. (A) Cell viability of MCF-7 cells treated with the indicated concentrations of Que for 24 and 48 h, as determined by the Cell Cycle Kit-8 assay. (B) mRNA expression levels of <t>ABCB1,</t> ABCC2 and ABCG2 following Que treatment. (C) Representative western blotting images, (D) protein expression levels of ABCB1, ABCC2 and ABCG2, and (E) Bax, Bcl-2, and cleaved caspase-3 were assessed by western blotting. (F) Representative images of flow cytometry and (G) apoptosis rate was analyzed by flow cytometry after Annexin V-FITC/PI staining. Data are presented as the mean ± SEM of at least three independent experiments. Statistical significance was determined by one/two-way ANOVA followed by Bonferroni's post hoc test for multiple comparisons. *P<0.05, **P<0.01 compared with the control group, ## P<0.01 compared with the Que (24 h) group. Que, Quercetin; Ctrl, control.
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    Cusabio abcb1
    Effects of Que on cell viability, mRNA levels, apoptosis and protein expression in MCF-7 cells. (A) Cell viability of MCF-7 cells treated with the indicated concentrations of Que for 24 and 48 h, as determined by the Cell Cycle Kit-8 assay. (B) mRNA expression levels of <t>ABCB1,</t> ABCC2 and ABCG2 following Que treatment. (C) Representative western blotting images, (D) protein expression levels of ABCB1, ABCC2 and ABCG2, and (E) Bax, Bcl-2, and cleaved caspase-3 were assessed by western blotting. (F) Representative images of flow cytometry and (G) apoptosis rate was analyzed by flow cytometry after Annexin V-FITC/PI staining. Data are presented as the mean ± SEM of at least three independent experiments. Statistical significance was determined by one/two-way ANOVA followed by Bonferroni's post hoc test for multiple comparisons. *P<0.05, **P<0.01 compared with the control group, ## P<0.01 compared with the Que (24 h) group. Que, Quercetin; Ctrl, control.
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    A schematic diagram illustrates the mechanistic pathway of Aβ accumulation and clearance in Alzheimer’s disease in relation to <t>ABCB1</t> genotype. Oxidative stress (ROS, lipid peroxidation, mitochondrial dysfunction) and neuroinflammatory signaling (IL-1β, NLRP3 inflammasome activation) trigger intracellular cascades such as NF-κB , MAPK/ERK , PI3K/Akt , and JNK , which downregulate or impair ABCB1 activity at the blood-brain barrier (BBB), thereby reducing Aβ efflux and promoting its accumulation within brain tissue. NF-κB activation through RAGE–Aβ interaction further amplifies inflammatory suppression of ABCB1 , creating a feed-forward loop of Aβ deposition. In contrast, protective pathways, including nuclear receptor signaling ( PXR ) and antioxidant defense via Nrf2 , upregulate ABCB1 transcription and enhance efflux function, facilitating Aβ clearance. The impact of genetic variation is highlighted by the difference between wild-type ABCB1 (3435C allele) and mutant-type (3435T allele). In wild-type ABCB1 (3435C allele), transporter activity is preserved, supporting effective clearance, whereas the ABCB1 3435C>T (rs1045642) polymorphism impairs expression and function, leading to reduced efflux and greater amyloid accumulation in the brain. Together, these regulatory mechanisms integrate environmental stressors, transcriptional control, and genetic polymorphism to determine the balance between Aβ clearance and deposition in the Alzheimer’s brain. Abbreviations: ABCB1 ATP-binding cassette subfamily B member 1, ROS reactive oxygen species, IL1β interleukin 1β, NLRP3 NOD-LRR and pyrin domain-containing protein 3, MDA malondialdehyde, NF-κB nuclear factor kappa β, PI3K phosphatidylinositol-3-phosphate, PXR pregnane X receptor, Nrf2 nuclear erythroid factor 2, BBB blood-brain barrier, RAGE receptor for advanced glycation end products, ATP adenosine-3-phosphate, ADP adenosine-3-phosphate, P phosphate
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    Image Search Results


    Effects of Que on cell viability, mRNA levels, apoptosis and protein expression in MCF-7 cells. (A) Cell viability of MCF-7 cells treated with the indicated concentrations of Que for 24 and 48 h, as determined by the Cell Cycle Kit-8 assay. (B) mRNA expression levels of ABCB1, ABCC2 and ABCG2 following Que treatment. (C) Representative western blotting images, (D) protein expression levels of ABCB1, ABCC2 and ABCG2, and (E) Bax, Bcl-2, and cleaved caspase-3 were assessed by western blotting. (F) Representative images of flow cytometry and (G) apoptosis rate was analyzed by flow cytometry after Annexin V-FITC/PI staining. Data are presented as the mean ± SEM of at least three independent experiments. Statistical significance was determined by one/two-way ANOVA followed by Bonferroni's post hoc test for multiple comparisons. *P<0.05, **P<0.01 compared with the control group, ## P<0.01 compared with the Que (24 h) group. Que, Quercetin; Ctrl, control.

    Journal: Oncology Reports

    Article Title: Quercetin reduces expression of ATP-binding cassette transporters by regulating the PTEN/PI3K/AKT signaling pathway in breast cancer cells

    doi: 10.3892/or.2026.9068

    Figure Lengend Snippet: Effects of Que on cell viability, mRNA levels, apoptosis and protein expression in MCF-7 cells. (A) Cell viability of MCF-7 cells treated with the indicated concentrations of Que for 24 and 48 h, as determined by the Cell Cycle Kit-8 assay. (B) mRNA expression levels of ABCB1, ABCC2 and ABCG2 following Que treatment. (C) Representative western blotting images, (D) protein expression levels of ABCB1, ABCC2 and ABCG2, and (E) Bax, Bcl-2, and cleaved caspase-3 were assessed by western blotting. (F) Representative images of flow cytometry and (G) apoptosis rate was analyzed by flow cytometry after Annexin V-FITC/PI staining. Data are presented as the mean ± SEM of at least three independent experiments. Statistical significance was determined by one/two-way ANOVA followed by Bonferroni's post hoc test for multiple comparisons. *P<0.05, **P<0.01 compared with the control group, ## P<0.01 compared with the Que (24 h) group. Que, Quercetin; Ctrl, control.

    Article Snippet: Primary antibodies included PTEN (1:5,000; cat. no. ab267787), Bcl-2 (1:6,000; cat. no. ab196495), Bax (1:6,000; cat. no. ab32503) and ABCG2 (1:5,000; cat. no. ab108312) from Abcam; p-PI3K (p85) (1:2,000; cat. no. 4228), p-AKT (Ser473) (1:2,000; cat. no. 4060), cleaved caspase-3 (1:5,000; cat. no. 9664), ABCC2 (1:1,000; cat. no. 12559) and ABCB1 (1:2,000; cat. no. 13342) from Cell Signaling Technology, Inc.; and GAPDH (1:12,000; cat. no. 60004-1-Ig), PI3K (1:3,000; cat. no. 20584-1-AP), AKT (1:3,000; 10176-2-AP), Caspase-3 (1:3,000; 19677-1-AP) and β-actin (1:10,000; cat. no. 66009-1-Ig) from Proteintech Group, Inc. After incubation with HRP-conjugated secondary antibodies (1:10,000; cat. no. SA00001-1 and SA00001-2; Proteintech Group, Inc.), protein bands were visualized using an ECL reagent (Beijing Lanbolide Trading Co., Ltd.) and imaged with a ChemiDoc XRS+ system (Bio-Rad Laboratories, Inc.).

    Techniques: Expressing, Western Blot, Flow Cytometry, Staining, Control

    Effects of PTEN overexpression in MCF-7 cells. mRNA expression levels of (A) PTEN, (B) ABCB1, ABCC2, ABCG2, Bax and Bcl-2 following PTEN overexpression. (C) Representative western blotting images and protein expression levels of (D) ABCB1, ABCC2, ABCG2, (E) PTEN, Bax and Bcl-2 following PTEN overexpression. The results are presented as the mean ± SEM of at least three independent experiments and analyzed using one-way ANOVA followed by Bonferroni's post hoc test. *P<0.05, **P<0.01 compared with the Plvx-con group.

    Journal: Oncology Reports

    Article Title: Quercetin reduces expression of ATP-binding cassette transporters by regulating the PTEN/PI3K/AKT signaling pathway in breast cancer cells

    doi: 10.3892/or.2026.9068

    Figure Lengend Snippet: Effects of PTEN overexpression in MCF-7 cells. mRNA expression levels of (A) PTEN, (B) ABCB1, ABCC2, ABCG2, Bax and Bcl-2 following PTEN overexpression. (C) Representative western blotting images and protein expression levels of (D) ABCB1, ABCC2, ABCG2, (E) PTEN, Bax and Bcl-2 following PTEN overexpression. The results are presented as the mean ± SEM of at least three independent experiments and analyzed using one-way ANOVA followed by Bonferroni's post hoc test. *P<0.05, **P<0.01 compared with the Plvx-con group.

    Article Snippet: Primary antibodies included PTEN (1:5,000; cat. no. ab267787), Bcl-2 (1:6,000; cat. no. ab196495), Bax (1:6,000; cat. no. ab32503) and ABCG2 (1:5,000; cat. no. ab108312) from Abcam; p-PI3K (p85) (1:2,000; cat. no. 4228), p-AKT (Ser473) (1:2,000; cat. no. 4060), cleaved caspase-3 (1:5,000; cat. no. 9664), ABCC2 (1:1,000; cat. no. 12559) and ABCB1 (1:2,000; cat. no. 13342) from Cell Signaling Technology, Inc.; and GAPDH (1:12,000; cat. no. 60004-1-Ig), PI3K (1:3,000; cat. no. 20584-1-AP), AKT (1:3,000; 10176-2-AP), Caspase-3 (1:3,000; 19677-1-AP) and β-actin (1:10,000; cat. no. 66009-1-Ig) from Proteintech Group, Inc. After incubation with HRP-conjugated secondary antibodies (1:10,000; cat. no. SA00001-1 and SA00001-2; Proteintech Group, Inc.), protein bands were visualized using an ECL reagent (Beijing Lanbolide Trading Co., Ltd.) and imaged with a ChemiDoc XRS+ system (Bio-Rad Laboratories, Inc.).

    Techniques: Over Expression, Expressing, Western Blot

    Effects of combined PTEN overexpression and Que treatment on ABC transporters and the PI3K/AKT signaling pathway in MCF-7 cells. mRNA expression levels of (A) ABCB1, (B) ABCC2 (C) and ABCG2 in different treatment groups. (D) Representative images and (E) protein expression levels of ABCB1, ABCC2, ABCG2, (F) p-PI3K, and (G) p-AKT were evaluated by western blotting. The results are presented as the mean ± SEM of at least three independent experiments and analyzed using one-way ANOVA followed by Bonferroni's post hoc test. *P<0.05, **P<0.01, ***P<0.001 compared with the Plvx-con group. Que, Quercetin; con, control; p, phosphorylated.

    Journal: Oncology Reports

    Article Title: Quercetin reduces expression of ATP-binding cassette transporters by regulating the PTEN/PI3K/AKT signaling pathway in breast cancer cells

    doi: 10.3892/or.2026.9068

    Figure Lengend Snippet: Effects of combined PTEN overexpression and Que treatment on ABC transporters and the PI3K/AKT signaling pathway in MCF-7 cells. mRNA expression levels of (A) ABCB1, (B) ABCC2 (C) and ABCG2 in different treatment groups. (D) Representative images and (E) protein expression levels of ABCB1, ABCC2, ABCG2, (F) p-PI3K, and (G) p-AKT were evaluated by western blotting. The results are presented as the mean ± SEM of at least three independent experiments and analyzed using one-way ANOVA followed by Bonferroni's post hoc test. *P<0.05, **P<0.01, ***P<0.001 compared with the Plvx-con group. Que, Quercetin; con, control; p, phosphorylated.

    Article Snippet: Primary antibodies included PTEN (1:5,000; cat. no. ab267787), Bcl-2 (1:6,000; cat. no. ab196495), Bax (1:6,000; cat. no. ab32503) and ABCG2 (1:5,000; cat. no. ab108312) from Abcam; p-PI3K (p85) (1:2,000; cat. no. 4228), p-AKT (Ser473) (1:2,000; cat. no. 4060), cleaved caspase-3 (1:5,000; cat. no. 9664), ABCC2 (1:1,000; cat. no. 12559) and ABCB1 (1:2,000; cat. no. 13342) from Cell Signaling Technology, Inc.; and GAPDH (1:12,000; cat. no. 60004-1-Ig), PI3K (1:3,000; cat. no. 20584-1-AP), AKT (1:3,000; 10176-2-AP), Caspase-3 (1:3,000; 19677-1-AP) and β-actin (1:10,000; cat. no. 66009-1-Ig) from Proteintech Group, Inc. After incubation with HRP-conjugated secondary antibodies (1:10,000; cat. no. SA00001-1 and SA00001-2; Proteintech Group, Inc.), protein bands were visualized using an ECL reagent (Beijing Lanbolide Trading Co., Ltd.) and imaged with a ChemiDoc XRS+ system (Bio-Rad Laboratories, Inc.).

    Techniques: Over Expression, Expressing, Western Blot, Control

    Effects of combined LY294002 and Que treatment on apoptosis and protein expression in MCF-7 cells. (A) Representative western blotting images and Protein expression levels of (B) ABCB1, ABCC2, ABCG2, (C) p-PI3K (D) PTEN, Bax, Bcl-2 and (E) p-AKT in different treatment groups. (F) mRNA expression levels of ABCB1, ABCC2, ABCG2, PTEN, Bax and Bcl-2 in different treatment groups. (G) Representative immunofluorescence images of ABCG2 expression (green). Nuclei were counterstained with DAPI (blue). Scale bar, 50 µm. (H) Representative flow cytometry images and (I) Apoptosis rate was analyzed by flow cytometry after Annexin V-FITC/PI staining. The results are presented as the mean ± SEM of at least three independent experiments and analyzed using two-way ANOVA followed by Bonferroni's post hoc test. *P<0.05, **P<0.01 compared with the control group; ## P<0.05 compared with the Que group. Que, Quercetin; Ctrl, control; p, phosphorylated.

    Journal: Oncology Reports

    Article Title: Quercetin reduces expression of ATP-binding cassette transporters by regulating the PTEN/PI3K/AKT signaling pathway in breast cancer cells

    doi: 10.3892/or.2026.9068

    Figure Lengend Snippet: Effects of combined LY294002 and Que treatment on apoptosis and protein expression in MCF-7 cells. (A) Representative western blotting images and Protein expression levels of (B) ABCB1, ABCC2, ABCG2, (C) p-PI3K (D) PTEN, Bax, Bcl-2 and (E) p-AKT in different treatment groups. (F) mRNA expression levels of ABCB1, ABCC2, ABCG2, PTEN, Bax and Bcl-2 in different treatment groups. (G) Representative immunofluorescence images of ABCG2 expression (green). Nuclei were counterstained with DAPI (blue). Scale bar, 50 µm. (H) Representative flow cytometry images and (I) Apoptosis rate was analyzed by flow cytometry after Annexin V-FITC/PI staining. The results are presented as the mean ± SEM of at least three independent experiments and analyzed using two-way ANOVA followed by Bonferroni's post hoc test. *P<0.05, **P<0.01 compared with the control group; ## P<0.05 compared with the Que group. Que, Quercetin; Ctrl, control; p, phosphorylated.

    Article Snippet: Primary antibodies included PTEN (1:5,000; cat. no. ab267787), Bcl-2 (1:6,000; cat. no. ab196495), Bax (1:6,000; cat. no. ab32503) and ABCG2 (1:5,000; cat. no. ab108312) from Abcam; p-PI3K (p85) (1:2,000; cat. no. 4228), p-AKT (Ser473) (1:2,000; cat. no. 4060), cleaved caspase-3 (1:5,000; cat. no. 9664), ABCC2 (1:1,000; cat. no. 12559) and ABCB1 (1:2,000; cat. no. 13342) from Cell Signaling Technology, Inc.; and GAPDH (1:12,000; cat. no. 60004-1-Ig), PI3K (1:3,000; cat. no. 20584-1-AP), AKT (1:3,000; 10176-2-AP), Caspase-3 (1:3,000; 19677-1-AP) and β-actin (1:10,000; cat. no. 66009-1-Ig) from Proteintech Group, Inc. After incubation with HRP-conjugated secondary antibodies (1:10,000; cat. no. SA00001-1 and SA00001-2; Proteintech Group, Inc.), protein bands were visualized using an ECL reagent (Beijing Lanbolide Trading Co., Ltd.) and imaged with a ChemiDoc XRS+ system (Bio-Rad Laboratories, Inc.).

    Techniques: Expressing, Western Blot, Immunofluorescence, Flow Cytometry, Staining, Control

    A schematic diagram illustrates the mechanistic pathway of Aβ accumulation and clearance in Alzheimer’s disease in relation to ABCB1 genotype. Oxidative stress (ROS, lipid peroxidation, mitochondrial dysfunction) and neuroinflammatory signaling (IL-1β, NLRP3 inflammasome activation) trigger intracellular cascades such as NF-κB , MAPK/ERK , PI3K/Akt , and JNK , which downregulate or impair ABCB1 activity at the blood-brain barrier (BBB), thereby reducing Aβ efflux and promoting its accumulation within brain tissue. NF-κB activation through RAGE–Aβ interaction further amplifies inflammatory suppression of ABCB1 , creating a feed-forward loop of Aβ deposition. In contrast, protective pathways, including nuclear receptor signaling ( PXR ) and antioxidant defense via Nrf2 , upregulate ABCB1 transcription and enhance efflux function, facilitating Aβ clearance. The impact of genetic variation is highlighted by the difference between wild-type ABCB1 (3435C allele) and mutant-type (3435T allele). In wild-type ABCB1 (3435C allele), transporter activity is preserved, supporting effective clearance, whereas the ABCB1 3435C>T (rs1045642) polymorphism impairs expression and function, leading to reduced efflux and greater amyloid accumulation in the brain. Together, these regulatory mechanisms integrate environmental stressors, transcriptional control, and genetic polymorphism to determine the balance between Aβ clearance and deposition in the Alzheimer’s brain. Abbreviations: ABCB1 ATP-binding cassette subfamily B member 1, ROS reactive oxygen species, IL1β interleukin 1β, NLRP3 NOD-LRR and pyrin domain-containing protein 3, MDA malondialdehyde, NF-κB nuclear factor kappa β, PI3K phosphatidylinositol-3-phosphate, PXR pregnane X receptor, Nrf2 nuclear erythroid factor 2, BBB blood-brain barrier, RAGE receptor for advanced glycation end products, ATP adenosine-3-phosphate, ADP adenosine-3-phosphate, P phosphate

    Journal: Molecular Neurobiology

    Article Title: Investigating the Impact of ABCB1 3435C>T (rs1045642) Variant on Severity and Cognitive Decline in Egyptian Alzheimer’s Disease Patients

    doi: 10.1007/s12035-026-05789-w

    Figure Lengend Snippet: A schematic diagram illustrates the mechanistic pathway of Aβ accumulation and clearance in Alzheimer’s disease in relation to ABCB1 genotype. Oxidative stress (ROS, lipid peroxidation, mitochondrial dysfunction) and neuroinflammatory signaling (IL-1β, NLRP3 inflammasome activation) trigger intracellular cascades such as NF-κB , MAPK/ERK , PI3K/Akt , and JNK , which downregulate or impair ABCB1 activity at the blood-brain barrier (BBB), thereby reducing Aβ efflux and promoting its accumulation within brain tissue. NF-κB activation through RAGE–Aβ interaction further amplifies inflammatory suppression of ABCB1 , creating a feed-forward loop of Aβ deposition. In contrast, protective pathways, including nuclear receptor signaling ( PXR ) and antioxidant defense via Nrf2 , upregulate ABCB1 transcription and enhance efflux function, facilitating Aβ clearance. The impact of genetic variation is highlighted by the difference between wild-type ABCB1 (3435C allele) and mutant-type (3435T allele). In wild-type ABCB1 (3435C allele), transporter activity is preserved, supporting effective clearance, whereas the ABCB1 3435C>T (rs1045642) polymorphism impairs expression and function, leading to reduced efflux and greater amyloid accumulation in the brain. Together, these regulatory mechanisms integrate environmental stressors, transcriptional control, and genetic polymorphism to determine the balance between Aβ clearance and deposition in the Alzheimer’s brain. Abbreviations: ABCB1 ATP-binding cassette subfamily B member 1, ROS reactive oxygen species, IL1β interleukin 1β, NLRP3 NOD-LRR and pyrin domain-containing protein 3, MDA malondialdehyde, NF-κB nuclear factor kappa β, PI3K phosphatidylinositol-3-phosphate, PXR pregnane X receptor, Nrf2 nuclear erythroid factor 2, BBB blood-brain barrier, RAGE receptor for advanced glycation end products, ATP adenosine-3-phosphate, ADP adenosine-3-phosphate, P phosphate

    Article Snippet: The TaqMan allelic discrimination real-time PCR assay was utilized to determine the genotype for rs1045642 (Applied Biosystems, Thermo Fisher Scientific; Assay ID: C__7586657_20) together with TaqMan Genotyping Master Mix (Thermo Fisher Scientific; Cat. No. 4371355) in accordance with the manufacturer’s recommendations [ ].

    Techniques: Activation Assay, Activity Assay, Mutagenesis, Expressing, Control, Binding Assay

    Comparative distribution of ABCB1 3435C>T (rs1045642) genotypes (CC, TT, CT) between healthy controls and AD patients ( a ); AD patients with different CDR scales ( b ); AD patients with different grades of impaired cognitive disorders as measured by MMSE ( c ). Data are expressed as the percentage distribution of cases within each group. Statistical comparison was performed using the chi-square test: CDR Clinical Dementia Rating “CDR1 (0.5–2): mild dementia, CDR2 (> 2–< 3): moderate dementia, CDR3 (≥ 3): severe dementia”; MMSE Mini-Mental State Examination “MMSE (27–30): normal cognition, MMSE (21–26): mild cognitive impairment, MMSE (10–20): moderate cognitive impairment, MMSE (< 10): severe cognitive impairment”

    Journal: Molecular Neurobiology

    Article Title: Investigating the Impact of ABCB1 3435C>T (rs1045642) Variant on Severity and Cognitive Decline in Egyptian Alzheimer’s Disease Patients

    doi: 10.1007/s12035-026-05789-w

    Figure Lengend Snippet: Comparative distribution of ABCB1 3435C>T (rs1045642) genotypes (CC, TT, CT) between healthy controls and AD patients ( a ); AD patients with different CDR scales ( b ); AD patients with different grades of impaired cognitive disorders as measured by MMSE ( c ). Data are expressed as the percentage distribution of cases within each group. Statistical comparison was performed using the chi-square test: CDR Clinical Dementia Rating “CDR1 (0.5–2): mild dementia, CDR2 (> 2–< 3): moderate dementia, CDR3 (≥ 3): severe dementia”; MMSE Mini-Mental State Examination “MMSE (27–30): normal cognition, MMSE (21–26): mild cognitive impairment, MMSE (10–20): moderate cognitive impairment, MMSE (< 10): severe cognitive impairment”

    Article Snippet: The TaqMan allelic discrimination real-time PCR assay was utilized to determine the genotype for rs1045642 (Applied Biosystems, Thermo Fisher Scientific; Assay ID: C__7586657_20) together with TaqMan Genotyping Master Mix (Thermo Fisher Scientific; Cat. No. 4371355) in accordance with the manufacturer’s recommendations [ ].

    Techniques: Comparison

    Forest plot of odds ratios (OR) with 95% confidence intervals (CI) for associations between the ABCB1 3435C>T (rs1045642) genotype and clinical outcomes. Logistic regression analysis was performed using CC genotypes as reference categories. The CC genotype was significantly associated with a higher likelihood of being in the healthy control group versus Alzheimer’s disease (AD), having a lower Clinical Dementia Rating (CDR < 3), and achieving higher MMSE > 20 scores. ORs are plotted on a linear scale (0–40), with the dashed vertical line indicating the null value (OR = 1).

    Journal: Molecular Neurobiology

    Article Title: Investigating the Impact of ABCB1 3435C>T (rs1045642) Variant on Severity and Cognitive Decline in Egyptian Alzheimer’s Disease Patients

    doi: 10.1007/s12035-026-05789-w

    Figure Lengend Snippet: Forest plot of odds ratios (OR) with 95% confidence intervals (CI) for associations between the ABCB1 3435C>T (rs1045642) genotype and clinical outcomes. Logistic regression analysis was performed using CC genotypes as reference categories. The CC genotype was significantly associated with a higher likelihood of being in the healthy control group versus Alzheimer’s disease (AD), having a lower Clinical Dementia Rating (CDR < 3), and achieving higher MMSE > 20 scores. ORs are plotted on a linear scale (0–40), with the dashed vertical line indicating the null value (OR = 1).

    Article Snippet: The TaqMan allelic discrimination real-time PCR assay was utilized to determine the genotype for rs1045642 (Applied Biosystems, Thermo Fisher Scientific; Assay ID: C__7586657_20) together with TaqMan Genotyping Master Mix (Thermo Fisher Scientific; Cat. No. 4371355) in accordance with the manufacturer’s recommendations [ ].

    Techniques: Control