Anti-Human CD243 (ABCB1) PerCP-eFluor
- Known as:
- Antibody toHuman CD243 (ABCB1) PerCP-eFluor
- Catalog number:
- 46-2439-41
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD243 (ABCB1) PerCP-eFluor
Related genes to: Anti-Human CD243 (ABCB1) PerCP-eFluor
- Gene:
- ABCB1 NIH gene
- Name:
- ATP binding cassette subfamily B member 1
- Previous symbol:
- PGY1, MDR1, CLCS
- Synonyms:
- P-gp, CD243, GP170, ABC20
- Chromosome:
- 7q21.12
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2015-11-13
- Gene:
- ABCB10P1 NIH gene
- Name:
- ABCB10 pseudogene 1
- Previous symbol:
- ABCB10P, ABCB10P2
- Synonyms:
- M-ABC2, MABC2
- Chromosome:
- 15q11.2
- Locus Type:
- pseudogene
- Date approved:
- 2001-07-13
- Date modifiied:
- 2018-05-23
Related products to: Anti-Human CD243 (ABCB1) PerCP-eFluor
Related articles to: Anti-Human CD243 (ABCB1) PerCP-eFluor
- The ectoparasitic mite Varroa destructor is the gravest threat to managed honeybees, and its control relies on a limited number of chemical miticides. Among these, amitraz is widely used because of its strong efficacy against mites and relatively low toxicity to bees. However, increasing resistance to amitraz in Varroa populations threatens its long-term effectiveness. While mutations in the mite's β2 octopamine receptor are strongly associated with amitraz resistance, additional mechanisms influencing toxicant uptake and efflux are believed to also contribute. ATP-binding cassette (ABC) transporters, including ABCB1/P-glycoproteins, are well-established mediators of xenobiotic efflux and pesticide tolerance across arthropods, making them promising targets for silencing via RNA interference (RNAi) to combat miticide resistance. - Source: PubMed
Publication date: 2026/06/03
Ricigliano Vincent AFine Julia DMueller RebeccaRivera LauraLitsey Eliza MLucadello Michelle CRinkevich Frank DRector Brian GNicklisch Sascha C T - Relapse in acute myeloid leukemia (AML) frequently arises from therapy-resistant cells persisting within the bone marrow microenvironment. This study investigated stromal interactions and signaling pathway dependencies regulating cytarabine (AraC) response during AML progression and resistance acquisition. - Source: PubMed
Publication date: 2026/06/02
Sharma AmitAnand TrishnaBhattacharyya JinaDas DamodarJaganathan Bithiah Grace - Drug resistance frequently results in treatment failure for leukemia and leads to the progression of chronic myeloid leukemia (CML) into an accelerated or blast phase. An increasing number of CML cases exhibit reduced responsiveness or are refractory to tyrosine kinase inhibitors and chemotherapeutic drugs. Exosomes, as intercellular communication carriers, have been shown to participate in various forms of tumor drug resistance, but their role and mechanisms in CML drug resistance have not yet been fully investigated. - Source: PubMed
Publication date: 2026/06/01
Li FeiLin Jin-FeiTian PengChen HaishengYang QianGuo QiqiWang JiashengHe YueChen JunruHu XiaojianLi ChunmouMai WeitongDuan MenghanPeng MichaelRousseau ZackaryChen ChunNi HeyuZhang Qing - Lung adenocarcinoma (LUAD) is a leading cause of cancer-related mortality, with hypoxia contributing to tumor progression and treatment resistance. Identifying hypoxia-related biomarkers could enhance prognosis and therapeutic strategies for LUAD. - Source: PubMed
Publication date: 2026/06/03
Alghamdi BandarRocha Sonia - Multidrug resistance mediated by ATP-binding cassette transporter B1 (ABCB1) remains a major obstacle in nonsmall cell lung cancer (NSCLC) therapy. While its role in drug efflux is well established, whether elevated ABCB1 expression is associated with broader immune-related phenotypes has not been completely elucidated. Here, we examined hABCB1-overexpressing and drug-adapted NSCLC models to assess coordinated changes in drug resistance and immune susceptibility. Increased ABCB1 expression was associated with enhanced efflux activity and reduced sensitivity to chemotherapeutic agents. Across engineered and drug-selected systems, ABCB1-high cells showed decreased susceptibility to NK-92-mediated cytotoxicity. Pharmacological inhibition of transporter activity partially increased effector-mediated killing, supporting ABCB1 activity as a contributing factor, while indicating that additional mechanisms may also be involved. Proteomic and cytokine profiling suggested coordinated alterations in inflammatory and interferon-related signaling pathways. In a human lung cancer tissue microarray, elevated hABCB1 expression was inversely associated with CD3 T-cell infiltration. Together, these findings support an association between elevated ABCB1 expression and both drug-resistance features and immune-related phenotypes in NSCLC. Further genetic and in vivo studies are required to define mechanistic causality and clinical relevance. - Source: PubMed
Publication date: 2026/05/11
Min Jin YoungKim Hye MinBang GeulJung Hae WonKim Yea JinLee Sang-YeopKim Dong JoonHa Sang KeunKim Lam Truc NgocHong Kwan SooJeong Hye GwangKim Jin HeeHan Eun Hee