ABCB5
- Known as:
- ABCB5
- Catalog number:
- 000899A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCB5
Related genes to: ABCB5
- Gene:
- ABCB5 NIH gene
- Name:
- ATP binding cassette subfamily B member 5
- Previous symbol:
- -
- Synonyms:
- EST422562, ABCB5beta, ABCB5alpha
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2016-10-05
Related products to: ABCB5
Related articles to: ABCB5
- Renal cell carcinoma (RCC) is frequently resistant to tyrosine kinase inhibitors (TKIs) such as sunitinib, limiting therapeutic efficacy. ATP-binding cassette (ABC) transporters, including ABCB1, ABCB5, and ABCG2, are important transporters implicated in multidrug resistance, influencing drug efflux and tumor progression. We aimed to evaluate the expression of ABCB1, ABCB5, and ABCG2 in human RCC tissues and human renal cancer cell lines CAKI-2 and A-498, and to investigate their potential association with sunitinib resistance and associated signaling pathways. Twenty paired tumorous and adjacent non-tumorous human kidney tissue samples were analyzed for ABC transporter gene expression using qRT-PCR. RCC cell lines CAKI-2 and A-498, including sunitinib-resistant derivatives, were treated with 40 µM sunitinib. The levels of transporters and key signaling proteins were assessed by Western blot. ABCG2 was consistently higher in tumorous tissues, and ABCB1 and ABCB5 showed grade-dependent increases in tumors. Resistant cells exhibited elevated ABCB1 and dynamic ABCB5 and ABCG2 expression patterns compared to sensitive cells, indicating an association between altered transporter expression and the resistant phenotype. Sunitinib treatment modulated signaling pathways, with differential activation of PI3K/Akt, NF-κB, and MAPK/ERK observed in sensitive versus resistant cells. Our findings suggest that altered ABCB1 and ABCG2 expression may be associated with the development of sunitinib resistance in RCC and may be linked to changes in key survival signaling pathways. These findings provide a basis for future functional studies investigating the role of ABC transporters in sunitinib resistance and may contribute to the development of personalized therapeutic strategies in RCC. - Source: PubMed
Publication date: 2026/07/21
Vass AnnaKirály JózsefSzabó ErzsébetKónya GáborShammas AliSzegedi KrisztiánDezső BalázsJuhász ÉvaHalmos GáborSzabó Zsuzsanna - Uveal melanoma (UM) is a deadly ocular malignancy with well-described genetic alterations that predict disease outcome. However, our current understanding of the biological underpinnings of high-risk uveal melanoma progression remains relatively limited. Using RNA expression profiles from 250 patients with UM, we identified 12 novel biomarkers associated with high-risk UM, with protein expression level validation of the top two candidates: the transcriptional regulator RBFOX2 and matrix protein COL9A3. Moreover, we investigated the functional contribution of COL9A3 via its overexpression in EIF1AX and BAP1 UM cell lines. Our data suggest that COL9A3 enhances cell motility and cell proliferation and alters morphology specifically in BAP1 UM cells. Furthermore, zebrafish xenograft studies revealed increased cell dissemination in a EIF1AX UM cell line upon overexpression of COL9A3, whereas a BAP1 UM cell line remained unchanged under wild-type conditions. Interestingly, RNA sequencing revealed a high-stress profile by upregulated metabolic activity and loss of protein translation due to COL9A3 overexpression. BAP1 UM appears to adapt to this stress by upregulation of plasticity markers, such as CD44, Nestin, EZH2, ABCB5, PAX3 and CD166, as a coping mechanism. These markers are known as differentiation markers during the development of melanocyte biogenesis and are implicated in plasticity in other high-risk cancers. The relationship between COL9A3 and plasticity was validated by multiplex immunohistochemistry of formalin-fixed paraffin-embedded (FFPE) tissue, which demonstrated colocalization of COL9A3, CD44 and Nestin. BAP1-UM samples presented higher levels of COL9A3, CD44 and Nestin expression than EIF1AX or SF3B1 UM samples based on the mean fluorescent intensity of each marker. A positive correlation between COL9A3 and Nestin expression in triple-positive cells, irrespective of the UM subtype, was observed. Collectively, our findings suggest that COL9A3 is a novel high-risk biomarker that may contribute to UM cell plasticity and is most prevalent in BAP1 UM. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/07/21
van den Bosch QccVerdijk R MFadlelseed Hvan den Bosch TppOwens SKennedy SKilic EBrosens E - ABCB5+ dermal mesenchymal stem cells (DMSCs) regulate macrophage activation via interleukin-1 receptor antagonist (IL-1Ra), but upstream control mechanisms remain unclear. Here, we define a dual-signal model integrating inflammatory and type 2 cytokine pathways. IFNγ/LPS priming initiates IL-1Ra expression, while IL-4 signaling through IL-4Rα amplifies this response via STAT6 in both ABCB5+ DMSCs and macrophages. In coculture, ABCB5+ DMSCs drive macrophage polarization toward a CD206+/CD163+ phenotype with enrichment of CD163-expressing subsets. IL-4Rα blockade with dupilumab inhibits STAT6 activation, suppresses IL-1Ra amplification, and attenuates expansion of this IL-4Rα-dependent macrophage population. Collectively, these findings identify IL-4/IL-4Rα/STAT6 signaling as a conserved amplifier of IL-1Ra-mediated stromal-immune crosstalk. - Source: PubMed
Publication date: 2026/07/08
Singh KarmveerWilson Brian JWaaga-Gasser Ana MariaSchatz SusanneHainzl AdelheidYeung Philip CMaity PallabFrank Natasha YScharffetter-Kochanek KarinFrank Markus H - Patient-derived tumor xenograft (PDTX) models are considered the gold standard for preserving tumor heterogeneity and recapitulating patient drug responses, yet their use is limited by high cost, long timelines, and variable engraftment success. Here, we present the application of a soft lithography patterned polyacrylamide microtumor array platform designed to mimic biophysical aspects of the melanoma tumor microenvironment, including physiological stiffness, extracellular matrix (ECM) composition, and spatial confinement, which together recapitulate in vivo drug sensitivity for the evaluation of therapeutics. The microtumor array platform is comprised of approximately 100 distinct features per well, with a diameter of approximately 350 μm per feature, each imposing spatial confinement with peripheral geometric cues to confined cells. Using two BRAF mutant melanoma cell lines, Mela14 (treatment-resistant) and Mela16 (treatment-naïve), we investigated whether microtumor arrays could restore cancer stem cell (CSC) characteristics, using ABCB5 and CD271 marker expression, and recapitulate PDTX drug response phenotypes to the BRAF/MEK inhibitor combination dabrafenib/trametinib (DT). Immunofluorescence analysis revealed that CSC marker expression was diminished on conventional tissue culture plastic (TCP) but restored to levels comparable to primary and PDTX tissue upon five days of spiral-patterned hydrogel confinement. Drug response assays demonstrated that microtumor array primed Mela14 cells retained DT resistance, whereas Mela16 cells remained responsive, paralleling PDTX outcomes. Global proteomics indicated that spiral confinement upregulated pathways in Mela14 associated with drug resistance, metastasis, cell repair and survival, while spiral patterned Mela16 showed upregulated pathways associated with cellular homeostasis and increased proteome plasticity. These findings suggest that polyacrylamide microtumor arrays can reproduce key features of the in vivo melanoma microenvironment, which may enable rapid, reproducible, and clinically relevant drug sensitivity testing. Therefore, this platform offers potential as a complementary preclinical model for personalized medicine and therapeutic discovery in cancer. - Source: PubMed
Publication date: 2026/06/17
Liu YilingPawlush Matthew LGleba Justyna JLambert Ella GWilliams Caitlin EStenzel Martina HCopland John AKilian Kristopher A - Cell size has been associated with stem and progenitor cell states across multiple tissues, yet its regulation in the human corneal epithelium remains incompletely understood. This study aimed to characterize cell-size differences among limbal and corneal epithelial cell populations defined by the limbal stem cell (LSC) marker ABCB5 and the transit-amplifying cell (TAC) marker BCAM, and to investigate the molecular regulators of progenitor cell size. ABCB5-positive LSCs and BCAM-positive TACs were identified and isolated by flow cytometry, and the mean cell size was estimated using forward scatter (FSC). As a result, ABCB5-positive LSCs were significantly smaller than ABCB5-negative limbal epithelial cells, and BCAM-positive TACs exhibited a smaller cell size than BCAM-negative cells, particularly in the limbus. Immunofluorescence staining showed that Yes-associated protein 1 (YAP1) and BCAM were co-expressed in basal epithelial cells in the human limbus and cornea. Expression of the YAP1 transcriptional target gene CYR61 was elevated in BCAM-positive limbal cells. SiRNA-mediated knockdown of YAP1 or BCAM in cultured human limbal epithelial cells resulted in a significant increase in cell size. These findings identify small cell size as a characteristic feature of limbal BCAM-positive TACs and demonstrate that progenitor cell size is regulated by YAP1 and BCAM, highlighting an interaction between physical cell properties and progenitor function in the corneal epithelium. - Source: PubMed
Publication date: 2026/05/13
Suzuki KoseiSato ShinriFrank Markus HFrank Natasha YSasamoto Yuzuru