BCRP1

Last update 08 May 2025

Basic Info

Synonyms

BCR pseudogene 1, BCR-1, BCRP1

Introduction-

100 Clinical Results associated with BCRP1

100 Translational Medicine associated with BCRP1

0 Patents (Medical) associated with BCRP1

420

Literatures (Medical) associated with BCRP1

01 Mar 2025·Brazilian Journal of Microbiology

Evaluation of biofilm formation and antimicrobial susceptibility (drug resistance) of Candida albicans isolates

Article

Author: Kumaran, K Senthil ; Nitha, B ; Alvarez, Loretta ; Sivasubramani, K

Candida albicans comprises over 80% of isolates from all forms of human candidiasis. Biofilm formation enhances their capacity to withstand therapeutic treatments. In addition to providing protection, biofilm formation by C. albicans enhances its pathogenicity. Understanding the fundamental mechanisms underlying biofilm formation is crucial to advance our understanding and treatment of invasive Candida infections. An initial screening of 57 Candida spp. isolates using CHROMagar Candida (CHROMagar) media revealed that 46 were C. albicans. Of these, 12 isolates (33.3%) had the capacity to form biofilms. These 12 isolates were subjected to multiple biochemical and physiological tests, as well as 18 S rRNA sequencing, to confirm the presence of C. albicans. Upon analysis of their sensitivity to conventional antifungal agents, the isolates showed varying resistance to terbinafine (91.6%), voriconazole (50%), and fluconazole (42%). Among these, only CD50 showed resistance to all antifungal agents. Isolate CD50 also showed the presence of major biofilm-specific genes such as ALS3, EFG1, and BCR1, as confirmed by PCR. Exposure of CD50 to gentamicin-miconazole, a commonly prescribed drug combination to treat skin infections, resulted in elevated levels of gene expression, with ALS3 showing the highest fold increase. These observations highlight the necessity of understanding the proteins involved in biofilm formation and designing ligands with potential antifungal efficacy.

11 Feb 2025·Blood Advances

RAPID-CRISPR: highly sensitive diagnostic assay for detection of PML::RARA isoforms in acute promyelocytic leukemia

Article

Author: Jain, Hasmukh ; Maity, Akash ; Sathyanarayanan, Amritha ; Gawde, Jitendra ; Kumar, Rohit ; Khattry, Navin ; Patkar, Nikhil ; Vora, Jesal ; Subramanian, P. G. ; Hasan, Syed K. ; Bagal, Bhausaheb ; Sengar, Manju

AbstractAcute promyelocytic leukemia (APL), distinguished by the presence of PML::RARA fusion transcript, is a medical emergency because of its high early death rate, which is preventable when diagnosed early. Current diagnostic methods are precise and reliable but are time intensive, require sophisticated instruments, and analytical expertise. This study has redefined APL identification by CRISPR system (RAPID-CRISPR) to rapidly (<3 hours) detect PML::RARA. APL cell lines (NB4 and UF-1) and bone marrow/peripheral blood samples from 74 patients with APL (66/8, retrospective/prospective) and 48 controls were included in the study. We used a DETECTR (DNA endonuclease-targeted CRISPR transreporter) assay to identify the bcr1, bcr2, and bcr3 PML::RARA isoforms. To ensure high specificity, we used PML::RARA–specific loop-mediated isothermal amplification (LAMP) primers, synthetic protospacer-adjacent motif sites, and isoform-specific CRISPR RNAs. RAPID-CRISPR recognized APL with 100% sensitivity and 100% specificity in an ambispective cohort of patient samples. Furthermore, our blinded validation approach to detect PML::RARA in an unbiased manner provides an additional layer in the diagnostic precision of APL. RAPID-CRISPR demonstrated superior sensitivity, detecting as few as 1 copy of PML::RARA compared with 10 copies by the gold-standard reverse transcriptase qualitative and quantitative polymerase chain reaction. The nucleic acid extraction–free protocol combined with the 1-step reverse transcriptase LAMP–based DETECTR followed by lateral flow readout makes the RAPID-CRISPR assay suitable for diagnosing APL in point-of-care settings. This simple, cost-effective tool, with its easy-to-read format, is particularly valuable in underresourced regions. The assay facilitates timely diagnosis and prompt administration of lifesaving therapies such as all-trans retinoic acid and arsenic trioxide in APL.

01 Feb 2025·Research in Microbiology

2-Chloromethyl anthraquinone inhibits Candida albicans biofilm formation by inhibiting the Ras1-cAMP-Efg1 pathway

Article

Author: Zuo, Ting ; Zhang, Haoying ; Wang, Ziqi ; Lu, Yuanyuan ; Liao, Jianmin ; Zhang, Qi

Candida albicans is an opportunistic pathogen, and the formation of its biofilm makes it resistant to traditional antifungal therapy. Anthraquinones have universal antibacterial activity. We evaluated the inhibitory effects of 2-chloromethyl anthraquinone on C. albicans adhesion, mycelial morphology transformation, and biofilm formation. The results showed that 2-chloromethyl anthraquinone could inhibit C. albicans adhesion, mycelium formation, and biofilm formation in a dose-dependent manner at 2 μg/mL. In addition, 2-chloromethyl anthraquinone significantly inhibited the expression of biofilm formation-related genes in C. albicans, including ALS1, CPH1, ECE1, HWP1, TEC1, BCR1, and UME6. In addition, Ras1-cAMP-Efg1 pathway-related genes (RAC1, CYR1, and TPK2) were also significantly down-regulated, indicating that the inhibitory effect of 2-chloromethyl anthraquinone on C. albicans biofilms may be related to the Ras1-cAMP-Efg1 signaling pathway. In summary, the results of this study confirmed the inhibitory mechanism of 2-chloromethyl anthraquinone on the virulence factors of C. albicans, which laid a theoretical foundation for its use as an anti-biofilm agent against C. albicans.

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