ABCC5
- Known as:
- ABCC5
- Catalog number:
- 000911A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCC5
Related genes to: ABCC5
- Gene:
- ABCC5 NIH gene
- Name:
- ATP binding cassette subfamily C member 5
- Previous symbol:
- -
- Synonyms:
- MRP5, SMRP, EST277145, MOAT-C
- Chromosome:
- 3q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2016-10-05
Related products to: ABCC5
Related articles to: ABCC5
- KRAS mutations are among the most common genetic alterations in colorectal cancer (CRC) and are strongly linked to poor prognosis and therapeutic resistance. However, current treatments targeting KRAS-mutated CRC have shown limited clinical efficacy. Argonaute 2 (AGO2) is a critical component in microRNA (miRNA)-mediated gene silencing complex, which is involved in the maturation of miRNAs and the regulation of target genes. It has been reported that mutated KRAS can interact with AGO2 and impair its function, thereby amplifying the oncogenic potency of mutant KRAS and accelerating tumor progression. To explore the therapeutic implications of this interaction, we developed a peptide inhibitor and engineered peptide-gold nanoparticles (Au-pep) that specifically disrupted KRAS-AGO2 interaction, which dramatically attenuated the malignant phenotype of KRAS-mutated CRC cells. Mechanistically, Au-pep-mediated disruption of the KRAS-AGO2 complex led to partial restoration of the miRNA expression landscape, with let‑7c‑5p emerging as the most significantly up‑regulated effector. As a result, restored let-7c-5p caused a significant down-regulation of key oncogenic drivers (KRAS, c-Myc and Bcl2) to suppress the growth of KRAS-mutated CRC cells and induce their apoptosis. Furthermore, this miRNA restoration conferred dual therapeutic benefits by sensitizing KRAS-mutated CRC cells to 5-fluorouracil (5-FU) via ABCC5 repression and augmenting immunotherapy responsiveness via PD-L1 down-regulation. Our findings, taken together, delineate a new therapeutic paradigm with significant translational potential for improving clinical outcomes in this recalcitrant patient population. - Source: PubMed
Publication date: 2026/08/20
Xie JingyiWang SimengLiu JuanZhang YanZhu HaixiaoCui RongrongYao YaoYu WeiHou Peng - - Source: PubMed
Publication date: 2026/08/08
Yu DongshengLi JiyeWei QianyiZhu ChunshengZhang XiaodanLi XiaopingGuo Danfeng - Impaired amyloid-β clearance at the blood-brain barrier (BBB) contributes to Alzheimer's disease (AD), yet the regulation of endothelial transport processes under neuroinflammatory conditions remains incompletely understood. Here, we investigated the time-dependent effects of interleukin-1β (IL-1β), interleukin-6 (IL-6) classical signaling directly via the membrane-bound IL-6 receptor, and IL-6 trans-signaling via the IL-6 /soluble IL-6 receptor complex (IL-6/sIL-6r) on ATP-binding cassette (ABC) transporter activity and expression in primary porcine brain endothelial cells (PBECs), and assessed intracellular accumulation of amyloid-β. Cytokine exposure did not affect PBEC viability. IL-1β induced a robust, time-dependent increase in ABCB1 activity and expression, whereas IL-6 produced a transient enhancement that was not sustained at 72 h. In contrast, IL-6 trans-signaling elicited a delayed but sustained increase in ABCB1 function and expression. IL-1β increased ABCG2 activity and expression at early time points, while IL-6 and IL-6/sIL-6r had minimal effects. Notably, IL-1β and IL-6 trans-signaling increased ABCC5 activity without detectable changes in protein expression. Cytokine-induced transporter modulation was associated with reduced intracellular amyloid-β accumulation. Pharmacological inhibition of ABC transporters increased intracellular amyloid-β levels, supporting a role for these transporters in endothelial amyloid-β handling. However, as transendothelial amyloid-β transport was not directly assessed, these findings should be interpreted as changes in intracellular amyloid-β accumulation rather than direct evidence of altered BBB clearance. These findings demonstrate signaling- and time-dependent regulation of BBB ABC transporters and reveal distinct effects of IL-6 classical signaling and IL-6 trans-signaling on endothelial transporter regulation. Collectively, these results highlight signaling context as an important determinant of BBB transport responses under neuroinflammatory conditions. - Source: PubMed
Publication date: 2026/07/15
Razmi Ahmad HPenny Jeffrey I - Cilostazol, a phosphodiesterase 3 inhibitor, causes intolerable headaches in over one third of patients, frequently leading to treatment discontinuation. We investigated whether ABCC5 variant rs7636910 (NM_005688.4:c.1146A > G) protects against cilostazol-induced headaches through altered cyclic nucleotide signalling. - Source: PubMed
Publication date: 2026/07/22
Lee Sung HeeKim So MyoungLee Dong-HwanHasanuzzaman MdPark DanbiRahaman Md IntazurLee SeokilGu YongchulKim Hye WonPark WonheeKim HyunhoBang Woo-DaePark JoonheePark YejinPark Hyun JuneLee JinuCho Sung KweonPark KyungsooLee Min GooLee Ji HyunLee Eun-JaeKim So Won - Lung cancer presents complex etiopathology involving a mix of genetic predispositions and environmental factors. The best treatment modality is surgical resection. However, it becomes ineffective in the advanced metastatic stage. Thus, cisplatin-based chemotherapy, though restricted by an intrinsic and/or acquired chemo-resistant phenotype, remains the first-line therapy for advanced non-small-cell cancer (NSCLC). - Source: PubMed
Publication date: 2026/07/20
Kryczka JolantaKryczka Jakub MateuszJanczewski ŁukaszShimida ShoFrączyk AndrzejKolesińska BeataBoncela JoannaBrzeziańska-Lasota Ewa