The study describes a novel retroviral vector, SF91m3, which improves the post-transcriptional processing of the MDR1 gene, leading to increased expression of the multidrug resistance efflux pump in human hematopoietic cells.

The study demonstrates that down-regulation of CIAPIN1 reverses multidrug resistance in breast cancer cells by reducing MDR1 expression and P-gp levels, thereby increasing sensitivity to chemotherapeutic agents.

Clitocine reverses P-gp associated multidrug resistance by down-regulating NF-κB, leading to reduced MDR1 expression and increased sensitivity to doxorubicin.

GSP reverses P-gp associated MDR by inhibiting P-gp function and expression through down-regulation of NF-κB and MAPK/ERK pathway mediated YB-1 activity.

miR-381 and miR-495 are down-regulated in MDR leukemia cells and negatively correlate with MDR1/P-gp expression, suggesting their role in modulating drug resistance.

The study demonstrates that silencing the MDR1 gene using siRNA reverses multidrug resistance in human hepatocellular carcinoma cells subline Bel-7402/ADM, particularly against adriamycin.

The study identifies mdr1 as a gene encoding P-glycoprotein that contributes to chemoresistance in EBV-T-LPDs by actively effluxing chemotherapeutic agents like etoposide and doxorubicin.

The study found that cyp51A and mdr1 genes were significantly overexpressed in voriconazole-resistant Aspergillus flavus isolates, suggesting their involvement in resistance mechanisms.

The study describes an endogenous overexpression system for multidrug transporters in Candida albicans, demonstrating the functional expression of Cdr1p and Mdr1p, along with the characterization of specific mutations affecting their substrate transport capabilities.

DCTPP1 knockdown increases sensitivity to 5-FU in gastric cancer cells by downregulating MDR1 expression through promoter hypermethylation.

Resveratrol (RES) and didox (DID) sensitize colorectal cancer cells to doxorubicin (DOX) by enhancing apoptosis and reducing P-glycoprotein (P-gp) efflux activity. MDR1 gene expression was not affected by RES or DID, but their ability to inhibit P-gp activity was confirmed.

The study identifies mutations in MRR1, TAC1, ERG11, and ERG7 that contribute to fluconazole resistance in Candida albicans, along with genomic alterations such as loss of heterozygosity and copy number variations.

The study shows that c-fos upregulates mdr1, leading to increased P-gp expression and enhanced efflux function, contributing to multidrug resistance in HEp-2 laryngeal cancer cells.

WBP2 interacts with ERα to enhance MDR1 transcription, leading to doxorubicin resistance in ERα-positive breast cancer cells.

Glucose starvation increases mitochondrial MDR1 expression, leading to metformin resistance in human malignant mesothelioma cells.

FLASH-NGS was developed for the detection of antimicrobial resistance genes and mutations in clinical samples, demonstrating high sensitivity and specificity for various pathogens including Staphylococcus aureus, Enterococcus faecium, and Plasmodium falciparum.

The study identified that CSDP + and fluconazole combination led to overexpression of MDR1 and MRR1 genes in C. albicans, suggesting their involvement in fluconazole resistance through efflux mechanisms.

Pygo2 overexpression was found to correlate with MDR1 expression and drug resistance in gastric cancer. Knockdown of Pygo2 reduced MDR1 expression and restored drug sensitivity.

Ganetespib showed excellent synergistic antifungal activity with flucytosine against azole-resistant C. albicans, down-regulating the expression of ERG11, CDR1, CDR2, and MDR1 genes.

Low glucose conditions enhance fluconazole resistance in Cryptococcus neoformans by increasing the expression of efflux pump genes AFR1 and AFR2, leading to increased efflux pump activity.

The study identified mutations in the MDR1 gene in Leishmania tropica isolates, which are associated with resistance to pentavalent antimonial compounds.

The study identified and characterized two full-length cDNAs of mdr1 and mdr2 genes in Mytilus galloprovincialis, which are involved in the multixenobiotic resistance system against okadaic acid.

The study investigated the role of ALDH1A1 in drug resistance in ovarian cancer cell lines. Knockout of ALDH1A1 affected the expression of MDR1/P-gp, BCRP, and COL3A1, influencing resistance to paclitaxel and topotecan.

The study identifies CDR1, MDR1, and ABC2 efflux pump genes as key contributors to azole resistance in Candida species. Both pantoprazole and haloperidol were effective in reducing fluconazole resistance by inhibiting these efflux pumps.

GemA is required for azole susceptibility, virulence, and cell wall integrity in Aspergillus fumigatus. Its deletion leads to increased resistance to azoles and terbinafine, likely through upregulation of drug efflux pumps.

The study identified cyp51A mutations TR34/L98H/S297T/F495I in strains AF1 and AF2, TR46/Y121F/T289A in strains AF4 and AF8, and no cyp51A mutation in strain AF5. Additionally, hmg1 mutation S541G was found in strains AF1 and AF2. Overexpression of genes associated with ergosterol synthesis and efflux pumps contributed to azole resistance.

ESR1 activating mutations (Y537S and D538G) confer chemoresistance to paclitaxel and doxorubicin through the JNK/c-Jun MDR1 pathway.

The study investigated the interaction of unsymmetrical bisacridines (UAs) with ABC transporters and their effects on cancer cell lines, showing that UAs are substrates for MDR1 and do not significantly influence the expression of ABC transporters in LS 174T and DU 145 cells.

Elacridar effectively inhibited P-gp activity and increased sensitivity to paclitaxel and doxorubicin in 2D cultures but not cisplatin. In 3D spheroids, P-gp activity inhibition was observed, but no re-sensitization to paclitaxel occurred.

The study identifies ERG11 overexpression as a key factor in fluconazole tolerance in Candida albicans isolates from head and neck cancer patients, highlighting its role in reducing susceptibility to fluconazole.

The study shows that 'silent' MDR1 genes in revertant cells can be activated through cell fusion with multidrug-resistant cells, leading to increased P-glycoprotein expression and multidrug resistance.

The study identifies the expression of mdr1 and mdr3 P-glycoproteins in acute and chronic leukemias, highlighting their potential role in drug resistance.