Ask about this productRelated genes to: ULBP1 antibody
- Gene:
- ULBP1 NIH gene
- Name:
- UL16 binding protein 1
- Previous symbol:
- -
- Synonyms:
- RAET1I
- Chromosome:
- 6q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2016-10-05
Related products to: ULBP1 antibody
Related articles to: ULBP1 antibody
- Flow-cytometric readouts in acute myeloid leukemia (AML) may depend on specimen source and processing. We assessed whether sample source (peripheral blood [PB] vs. bone marrow [BM]) and cryopreservation influence immune-evasion-related markers on AML blasts. Paired PB and BM samples from 19 adults were analyzed fresh and after cryopreservation. Viable CD45 singlets were assessed for ULBP1-6, MICA/B, CD34, CD44, CD70, CD80, and CD184 using median fluorescence intensity (MFI) and relative fluorescence index (RFI). Paired comparisons used two-sided Wilcoxon signed-rank tests with Benjamini-Hochberg correction across six markers within each endpoint and comparison. Discordance was also assessed using a predefined conventional 20% reference threshold. After adjustment, RFI did not differ between fresh and cryopreserved samples within PB or BM, or between fresh PB and BM. In cryopreserved samples, PB and BM differed for CD70 (q = 0.042) and ULBP1-6 (q = 0.028). Cryopreservation increased MFI for CD184 and ULBP1-6 in PB and BM and for MICA/B in PB; no PB-BM MFI difference remained significant. Threshold-based classification was discordant for CD34, CD44, CD80, CD184, MICA/B, and ULBP1-6 in 5.3-38.9% of pairs, whereas CD70 showed none. Cohort-level differences were limited to specific markers and conditions, while patient-level threshold discordance persisted. Sample source and cryopreservation should therefore be considered when interpreting threshold-based classifications. - Source: PubMed
Publication date: 2026/08/09
Richter SvenLeinauer BenediktThoma AliciaSchmälter Ann-KristinWaidhauser JohannaSchmid ChristophRank AndreasLöhr Phillip - KRAS mutation drives oncogenic progression and creates an immunosuppressive microenvironment in cancers like pancreatic ductal adenocarcinoma and colorectal cancer. We investigate the immunomodulatory mechanisms of the KRAS inhibition and its synergy with natural killer (NK) cell therapies. We demonstrate that KRAS inhibition with MRTX1133 remodels the immune landscape by reducing myeloid-derived suppressor cell (MDSC) accumulation and facilitating infiltration and activation of NK and CD8 T cells. Crucially, MRTX1133 reverses systemic immunosuppression, restoring the fitness of adoptively transferred NK cells. Mechanistically, KRAS inhibition impairs IFNGR1 palmitoylation and subsequent lysosomal degradation. MRTX1133 stabilizes IFNGR1 by reducing palmitoyltransferase expression and the palmitate pool. This stabilization increases IFN-γ/IFNGR signaling and up-regulates NK cell-activating ligands ICAM1 and ULBP1, thereby sensitizing cancer cells to NK cells. Consequently, combining MRTX1133 with IL-15 or adoptive NK cell therapy yields synergistic antitumor responses and prolonged survival. Our findings provide mechanistic rationale for combining KRAS inhibitors with NK cell-based immunotherapies to improve outcomes for patients with KRAS-mutant cancers. - Source: PubMed
Publication date: 2026/07/23
Hu TuoMo TaiweiWang LinKe QiuqingChi LiangjieChen HongyuanXu ChaoHuang ChenshenLin AipingCai ShaoxinChen HaiyuWang WenyuJin LongyangZhao JunzhangLiu HaoyunLiu ChuanyuanBaihetiyaer YimamuTuersun AbudumaimaitijiangAbulimiti AbuduhalikeZheng YanWang ZuweiChen ShiCao JieLu ShiyunHuang XuepingXue FangqinHe Chunbo - TB meningitis (TBM) has up to 50% mortality in people living with HIV. We investigated differences in cerebrospinal fluid (CSF) host immune responses associated with short-term mortality. - Source: PubMed
Publication date: 2026/06/18
Louine MartineauDandekar RaviReddy Sumanth PKaralius Mary CWaldrop GreerWang ShiyinGakuru JaneKimuda SarahMugabi TimothyMusubire Abdu KKagimu EnockAbassi MahsaKabahubya MableWilliams Darlisha APhan Hoang VanDai BiyueZia MahamZorn Kelsey CFouassier CamilleGerungan ChloeMarra Pedro SSkipper Caleb PBahr Nathan CLangelier Charles RCreswell Fiona VBoulware David RMeya David BWilson Michael R - Neuroblastoma (NB) is the most common extracranial solid tumor in children and remains a major therapeutic challenge in high-risk patients because of frequent recurrence and metastasis. γδT cells are a unique lymphocyte subset with potent antitumor activity and are widely distributed in NB tumors. However, the immunosuppressive tumor microenvironment limits γδT-cell effector function and promotes immune evasion. In this study, we found that ULBP1 expression was frequently down-regulated in NB tumor tissues and cell lines and that low ULBP1 expression was associated with high-risk clinical features and poor prognosis. Further investigation revealed that doxorubicin, a key chemotherapeutic agent used in NB treatment, up-regulated ULBP1 through down-regulating DNA methyltransferase 1 (DNMT1), thereby decreasing methylation of the ULBP1 promoter. This epigenetic modulation sensitized NB tumor cells to γδT-cell-mediated cytotoxicity in vitro and in vivo. Collectively, our findings uncover a novel mechanism by which doxorubicin enhances NB tumor susceptibility to γδT-cell-mediated killing through ULBP1 up-regulation. This study provides a strong rationale for combining chemotherapy with γδT-cell-based immunotherapy to improve outcomes in high-risk NB patients. - Source: PubMed
Wang HuiWang XiaolinYang WeiWang WeiChai WenjiaLiu XiangjunFeng JunYang ShenSong WenqiLi QiliangZhang HuiMou WenjunChen XiPei MengmiaoLu ZhengjingPeng YunSu YanYao XingfengWang HuanminGui Jingang - Cell targeting/permeabilization, organelle/biochemical pathway regulation, and drug resistance/metastasis/immunological expressions are considerations to advance cancer nanomedicine design. This study modulated mitochondria-targeting YKWYYRGAA (P1) peptide, into a multifunctional excipient via N-methylation and N-dimethylation, to synergise nano-chitosan conjugate in drug delivery and non-small cell lung cancer treatment. The spray-dried chitosan nanoparticles developed from P1, N-methylated YKWYYRGAA (P2) and N-dimethylated YKWYYRGAA (P3) were subjected to physicochemical testing, NRAS-mutated H1299 cell permeability/cytotoxicity/apoptosis and cell cycle arrest/drug resistance/metastasis/immunomodulation assessment, and in vivo pharmacokinetics/pharmacodynamics investigations. Methylated P2 increased cancer cell permeability/intracellular drug/nanoparticle uptake/drug targeting via sustained- and pH-stimuli responsive release and cytotoxicity unlike P1 and P3 which were ceased at membrane interface by excessive ionic/hydrophobic interactions. P2-grafted nanochitosan induced mitochondria-mediated apoptosis with minimal necrosis via ROS activation and FasL-linked death. It suppressed mTOR/MAPK signalling overcoming EGFR-resistance/EGFR mutation-independent pathways in tumorigenesis. It mitigated drug resistance via downregulating P-gp (efflux receptor) and GSTP1 (degrading enzyme) expressions, and epithelial-mesenchymal transition via interplay of E-cadherin against N-cadherin/snail/twist 1/vimentin/ezrin/MMP9 with MICA/ULBP1 suppression to reduce immunological lung tissue lysis. The inhaled P2-grafted nanochitosan provided a positive lung cancer recovery with reduced systemic exposure and hematological/biochemical toxicities. Single instead of dimethylation of YKWYYRGAA promoted the cascades of inter-dependent anti-cancer activities and efficacy of nanochitosan. - Source: PubMed
Publication date: 2026/05/10
Zaiki YazidChee Chin FeiAgeitos LuciaNaharudin IdanawatiZainudin Badrul HisyamLeong Lek MunJaime Rodriguez GonzálezJimenez CarlosGan Chee YuenTraini DanielaWong Tin Wui