abcb1  (Proteintech)

Journal: Biochemistry and Biophysics Reports

Article Title: TMEM207-mediated the impairment of skin regeneration through YAP sequestration in an allergic contact dermatitis model

doi: 10.1016/j.bbrep.2025.102409

Figure Lengend Snippet: (A): (left) Representative immunohistochemical staining of the skin using an anti -ABCB1 antibody. (center) Comparison of PPARg and SCD1 gene expression. (right) Representative immunohistochemical staining of the skin using an anti -SCD1 antibody. ∗∗ no significant difference; ∗P < 0.05. (B): Representative immunohistochemical staining of the skin using an anti -ki67 antibody and Nuclear Ki67 IHC score. Expression of ki67 was significantly reduced in Tg compared to wild type. ∗P < 0.05. (C): Representative immunohistochemical staining of the skin using an anti -Loricrin antibody. (D): Representative immunohistochemical staining of the skin using an anti-YAP antibody.

Article Snippet: Rabbit anti -GAPDH antibodies were obtained from Sigma-Aldrich (St. Louis, MO, USA), and rabbit anti -ABCB1, anti -SCD1, anti -NEDD4, anti -Ki67, anti -Loricrin, and anti-YAP antibodies were purchased from ProteinTech (Proteintech, Inc., USA).

Techniques: Immunohistochemical staining, Staining, Comparison, Gene Expression, Expressing

Journal: bioRxiv

Article Title: P-glycoprotein exofection between fetal and maternal cells as a mechanism of intercellular material transfer at the feto maternal interface

doi: 10.64898/2026.01.04.697556

Figure Lengend Snippet: (A) Immunohistochemical localization of P-gp in human fetal membrane tissues, showing the amnion epithelial layer (AEC), underlying chorionic trophoblast cells (CTCs), and maternal decidua. Representative control (left) and P-gp–stained sections (right) are shown at 10× magnification. (B) Schematic of the transwell configuration used for fetal membrane explant studies, with the fetal side oriented apically (left) or the maternal decidual side oriented apically (right). (C) Tacrolimus transport across fetal membrane explants quantified by LC–MS/MS, demonstrating directional efflux from the fetal to the maternal compartment. (D) Transwell systems using isolated CTCs (left) and DECs (right) to assess cell-specific transporter activity. (E) Tacrolimus efflux measured in CTC and DEC monolayers, showing higher efflux capacity in CTCs. (F) Relative ABCB1 mRNA expression in CTCs and DECs determined by qPCR. (G) Flow cytometric quantification of intracellular P-gp protein levels in DECs and CTCs using PE-conjugated antibody staining. Data are presented as mean ± SEM. Statistical analysis was performed using Student’s t-test. p < 0.05, p < 0.01, * p < 0.001.

Article Snippet: Total RNA (1 μg) was reverse-transcribed using a high-capacity RNA-to-cDNA kit (Applied Biosystems). qPCR reactions were performed using taqmanTM PCR master mix (Applied Biosystems) and taqmanTM gene expression assay (FAM) probes for ABCB1 HS00184500 (Life Technologies) with GAPDH (Life Technologies, Hs00177504) as internal control.

Techniques: Immunohistochemical staining, Membrane, Control, Staining, Liquid Chromatography with Mass Spectroscopy, Isolation, Activity Assay, Expressing

Journal: bioRxiv

Article Title: P-glycoprotein exofection between fetal and maternal cells as a mechanism of intercellular material transfer at the feto maternal interface

doi: 10.64898/2026.01.04.697556

Figure Lengend Snippet: (A) Pathway enrichment analysis of differentially expressed genes (DEGs) in LPS-treated DECs (left) and CTCs (right), showing robust activation of immune and inflammatory signaling pathways in DECs and minimal pathway induction in CTCs. (B) Volcano plots depicting significantly upregulated and downregulated genes in DECs (left) and CTCs (right). Key inflammatory mediators are highlighted. (C) Reactome analysis identifying transporter-related pathways altered by inflammation, including ABC transporter families, with ABCB1 downregulated in DECs and preserved or upregulated in CTCs. (D) Network analysis of upstream regulators and signaling molecules associated with ABCB1 expression under inflammatory conditions in DECs (left) and CTCs (right).

Article Snippet: Total RNA (1 μg) was reverse-transcribed using a high-capacity RNA-to-cDNA kit (Applied Biosystems). qPCR reactions were performed using taqmanTM PCR master mix (Applied Biosystems) and taqmanTM gene expression assay (FAM) probes for ABCB1 HS00184500 (Life Technologies) with GAPDH (Life Technologies, Hs00177504) as internal control.

Techniques: Activation Assay, Protein-Protein interactions, Expressing

Journal: bioRxiv

Article Title: P-glycoprotein exofection between fetal and maternal cells as a mechanism of intercellular material transfer at the feto maternal interface

doi: 10.64898/2026.01.04.697556

Figure Lengend Snippet: (A) Immunofluorescence analysis of P-gp expression in DECs under four treatment conditions: Control, LPS, EVs, and LPS + EVs. Nuclei were stained with DAPI (blue) and P-gp with a FITC-conjugated antibody (green). Images captured at 20× magnification. Quantification of P-gp mean fluorescence intensity is shown in the accompanying bar graph. (B) Functional assessment of P-gp activity using a calcein-AM efflux assay across the same conditions. Verapamil was used as a positive control to confirm efflux specificity. (C) Generation of transporter-deficient DECs using ABCB1-targeted siRNA. Knockdown efficiency was validated by qPCR. (D) Loss of P-gp–mediated efflux in knockdown (KD) cells confirmed by increased intracellular calcein accumulation. (E) Rescue of P-gp protein expression in P-gp–deficient DECs following treatment with CTC-derived EVs. Groups include siRNA control, P-gp KD, and P-gp KD + EVs. Representative immunofluorescence images and quantified fluorescence intensities illustrate EV-mediated restoration of P-gp protein. (F) Functional restoration of P-gp activity in KD cells following EV treatment, measured using a dye efflux assay. EV treatment significantly reduced dye accumulation relative to untreated KD cells, demonstrating recovery of transporter function. Statistical significance was determined using Student’s t -test or one-way ANOVA. Data are presented as Mean ± SEM. Significance is denoted as * for p < 0.05, ** for p < 0.01 and *** for p < 0.001

Article Snippet: Total RNA (1 μg) was reverse-transcribed using a high-capacity RNA-to-cDNA kit (Applied Biosystems). qPCR reactions were performed using taqmanTM PCR master mix (Applied Biosystems) and taqmanTM gene expression assay (FAM) probes for ABCB1 HS00184500 (Life Technologies) with GAPDH (Life Technologies, Hs00177504) as internal control.

Techniques: Immunofluorescence, Expressing, Control, Staining, Fluorescence, Functional Assay, Activity Assay, Positive Control, Knockdown, Derivative Assay

Journal: Oncology Research

Article Title: Utilization of a UPLC-MS/MS Approach to Elucidate the Role of ABCB1-Mediated Paclitaxel Resistance in Non-Small Cell Lung Cancer Cells

doi: 10.32604/or.2025.068967

Figure Lengend Snippet: ABCB1 is identified as a key factor promoting paclitaxel resistance in NSCLC cells. ( A ) CCK-8 assay showing efficacy of paclitaxel in NSCLC cells ( n = 3). ( B ) The difference in colony formation between A549 and A549/TAX cells ( n = 3). ( C ) The apoptotic rate of A549 and A549/TAX cells at the same paclitaxel concentration as determined by flow cytometry ( n = 3). ( D ) Volcano plot of differentially expressed genes. ( E ) Heatmap of the ABC family members in A549 and A549/TAX cells. ( F ) WB assay of P-glycoprotein expression in NSCLC cells ( n = 3). ** p < 0.01, *** p < 0.001. NS = not significant

Article Snippet: On the third day of cell culture, paclitaxel (1.6/8/40 μg/mL) or ABCB1 inhibitors (25 ng/mL tariquidar (MedChemExpress, Shanghai, China; Cat. No. HY-10550) or 1.5 μg/mL elacridar (MedChemExpress, Shanghai, China; Cat. No. HY-50879)) were added.

Techniques: CCK-8 Assay, Concentration Assay, Flow Cytometry, Expressing

Journal: Oncology Research

Article Title: Utilization of a UPLC-MS/MS Approach to Elucidate the Role of ABCB1-Mediated Paclitaxel Resistance in Non-Small Cell Lung Cancer Cells

doi: 10.32604/or.2025.068967

Figure Lengend Snippet: Roles of ABCB1, ABCC1 and ABCG2 in paclitaxel resistance in NSCLC. ( A ) The knockdown efficiency of ABCC1 in A549/TAX cells after knockdown by siRNA was verified by Western blot. ( B ) Cell viability of A549/TAX cells transfected with siNC or siABCC1 under treatment with various concentrations of paclitaxel was verified by the CCK-8 assay. ( C ) Western blot analysis comparing ABCG2 protein expression levels between A549 and A549/TAX cells. ( D ) Immunohistochemical staining of ABCB1 in clinical tissue samples of NSCLC. Case 1 and Case 2 were paclitaxel-sensitive NSCLC tissue. Case 3 and Case 4 were paclitaxel-resistant NSCLC tissues. Scale bar: 50 μm

Article Snippet: On the third day of cell culture, paclitaxel (1.6/8/40 μg/mL) or ABCB1 inhibitors (25 ng/mL tariquidar (MedChemExpress, Shanghai, China; Cat. No. HY-10550) or 1.5 μg/mL elacridar (MedChemExpress, Shanghai, China; Cat. No. HY-50879)) were added.

Techniques: Knockdown, Western Blot, Transfection, CCK-8 Assay, Expressing, Immunohistochemical staining, Staining

Journal: Oncology Research

Article Title: Utilization of a UPLC-MS/MS Approach to Elucidate the Role of ABCB1-Mediated Paclitaxel Resistance in Non-Small Cell Lung Cancer Cells

doi: 10.32604/or.2025.068967

Figure Lengend Snippet: Knockdown of ABCB1 sensitizes paclitaxel-resistant NSCLC cells. ( A ) WB assay of P-gp expression in A549/TAX cells transfected with siNC or siABCB1 ( n = 3). ( B ) qRT-PCR analysis of the mRNA levels of ABCB1 transfected with siNC or siABCB1 ( n = 3). ( C ) CCK-8 assay results showing the efficacy of paclitaxel in A549/TAX cells transfected with siABCB1 or siNC for 72 h ( n = 3). ( D ) WB assay of β-catenin and P-gp expression in NSCLC cells. ( E ) WB assay of SOX2 expression in NSCLC cells. *** p < 0.001. NS = not significant

Article Snippet: On the third day of cell culture, paclitaxel (1.6/8/40 μg/mL) or ABCB1 inhibitors (25 ng/mL tariquidar (MedChemExpress, Shanghai, China; Cat. No. HY-10550) or 1.5 μg/mL elacridar (MedChemExpress, Shanghai, China; Cat. No. HY-50879)) were added.

Techniques: Knockdown, Expressing, Transfection, Quantitative RT-PCR, CCK-8 Assay

Journal: Oncology Research

Article Title: Utilization of a UPLC-MS/MS Approach to Elucidate the Role of ABCB1-Mediated Paclitaxel Resistance in Non-Small Cell Lung Cancer Cells

doi: 10.32604/or.2025.068967

Figure Lengend Snippet: Synergistic effect of the P-gp inhibitors and paclitaxel. ( A ) Toxicity and safety of ABCB1 inhibitors (tariquidar and elacridar) were detected by CCK-8 assay ( n = 3). ( B ) IC 50 values of the combination of ABCB1 inhibitors (25 ng/mL tariquidar or 1.5 μg/mL elacridar) and paclitaxel were detected by CCK-8 assay ( n = 3). ( C ) Colony formation assay of ABCB1 inhibitors (25 ng/mL tariquidar or 1.5 μg/mL elacridar) combined with paclitaxel ( n = 3). ( D ) Apoptosis assay of ABCB1 inhibitors (25 ng/mL tariquidar or 1.5 μg/mL elacridar) combined with paclitaxel ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001. NS = not significant

Article Snippet: On the third day of cell culture, paclitaxel (1.6/8/40 μg/mL) or ABCB1 inhibitors (25 ng/mL tariquidar (MedChemExpress, Shanghai, China; Cat. No. HY-10550) or 1.5 μg/mL elacridar (MedChemExpress, Shanghai, China; Cat. No. HY-50879)) were added.

Techniques: CCK-8 Assay, Colony Assay, Apoptosis Assay

Journal: Oncology Research

Article Title: Utilization of a UPLC-MS/MS Approach to Elucidate the Role of ABCB1-Mediated Paclitaxel Resistance in Non-Small Cell Lung Cancer Cells

doi: 10.32604/or.2025.068967

Figure Lengend Snippet: A model depicting ABCB1-regulated paclitaxel resistance in NSCLC cells and detection by the UPLC/MS-MS method

Article Snippet: On the third day of cell culture, paclitaxel (1.6/8/40 μg/mL) or ABCB1 inhibitors (25 ng/mL tariquidar (MedChemExpress, Shanghai, China; Cat. No. HY-10550) or 1.5 μg/mL elacridar (MedChemExpress, Shanghai, China; Cat. No. HY-50879)) were added.

Techniques: Tandem Mass Spectroscopy