Ask about this productRelated genes to: CD38 antibody
- Gene:
- CD38 NIH gene
- Name:
- CD38 molecule
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4p15.32
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2014-11-18
Related products to: CD38 antibody
Related articles to: CD38 antibody
- Leukemic stem cells (LSCs) are the cellular reservoir most strongly implicated in relapse of acute myeloid leukemia, yet their operational detection by multiparameter flow cytometry remains challenging because of immunophenotypic overlap with normal progenitors and variability across assays. Including CD45RA in the CD34⁺CD38⁻ gating strategy substantially improves discrimination between malignant and normal stem/progenitor populations and thus enables more precise LSC enumeration in a single-tube format. Given the clinical importance of accurately quantifying the LSC compartment, we evaluated a refined single-tube flow cytometry assay that incorporates CD45RA within the CD34 + CD38- gate to increase specificity for the leukemic stem compartment. - Source: PubMed
Publication date: 2026/05/02
Navidinia Amir AbbasRostami ShahrbanooKarami NajibeShemshadinia MohammadrezaPatekhor Habibeh SabriHajaliaskari AkramMohammadi SaeedRostami TaherehBarkhordar MaryamVaezi MohammadJanbabaei GhasemChahardouli Bahram - The circadian rhythm system and sleep coordinate whole-body functions across the 24-h cycle, yet these rhythms progressively deteriorate with neurodegenerative diseases, including dementia. Growing evidence indicates that nicotinamide adenine dinucleotide (NAD) interacts with the circadian system through multiple molecular pathways and that NAD levels decline with dementia. In this review, we synthesize current evidence on the bidirectional relationship between NAD metabolism and circadian regulation in several dementia disorders, emphasizing the key circadian pathways, the nicotinamide phosphoribosyltransferase-mediated salvage synthesis, the NAD/sirtuins-dependent signaling, and the consumption of NAD by PARP1 and CD38. Finally, we also examine pharmacological and lifestyle strategies that target NAD, including NAD precursors, modulators of NAD biosynthetic and depleting enzymes, timed light and activity exposure, structured exercise programs, and dietary interventions. Overall, we focus on the bidirectional interplay between NAD metabolism and circadian rhythm regulation in dementia, with particular emphasis on how this interaction influences sleep and cognitive phenotypes across different dementia subtypes. Trial Registration: ClinicalTrials.gov identifier: NCT05040321, NCT04430517, NCT06971224, NCT05500170, NCT04070378. - Source: PubMed
Zhang Shi-QiLee JiyeonPan Jun-PingEnger RuneHrubos-Strøm HaraldMusiek Erik SFang Evandro FeiLe Weidong - BCR-ABL1-negative myeloproliferative neoplasms (MPNs) often exhibit overlapping clinical and morphological features, making accurate subcategorization challenging. The h-MICL (CD371) antigen, selectively expressed on leukemic stem cells (LSCs) and absent on CD34CD38 cells in normal or regenerating marrow, represents a potential diagnostic and prognostic marker. - Source: PubMed
Publication date: 2026/04/30
Oberoi GurleenDhawan RishiDass JasmitaGanju NehaViswanathan GaneshLata SumanAgarwal MukulKumar Pradeep KumarSeth TulikaMahapatra ManoranjanSaxena Renu - There is a critical need for development of non-invasive biomarkers of acute cellular rejection (ACR) in lung transplantation. We hypothesized that ACR induces changes in small extracellular vesicle (sEV) secretory output of T cells into the peripheral circulation, thereby providing a noninvasive method of diagnosis. First, we investigated this hypothesis in a mouse lung transplant model. In line with dense infiltration of lung allograft by T cells during ACR, peripheral blood total T cell and CD8 T cell counts, as well as, T cell sEV RNA cargoes (Cd3, Cd8, Ifng, Tcrb, and microRNA (Mir)21a) were significantly upregulated in mice receiving allogeneic compared to syngeneic lungs at the postoperative day 7 time point. Second, translating these findings to clinical lung transplantation, we analyzed circulating T cell sEV RNA cargoes with time-matched surveillance transbronchial allograft biopsies in 20 patients. In eight patients with >A1 ACR, eight candidate RNA biomarkers (CD8, TCR, IFNG, HLA-DRA, CD38, MIR21, MIRLET7I, MIR101) were significantly upregulated compared to 12 patients without ACR. Collectively, these findings support further investigation of T cell sEVs as a novel biomarker for ACR diagnosis in lung transplantation. - Source: PubMed
Publication date: 2026/04/28
Korutla LaxminarayanaMineura KatsutakaDeMarais NicoleLiu Charles RBurke VincentBai Yun ZhuHabertheuer AndreasHameed IrbazTerada YurikoTalapaneni SriharshaKawana ShinichiRitter Jon HKreisel DanielVallabhajosyula Prashanth - Although evidence links ferroptosis to tumor immunity, the rationale and translational potential of ferroptosis-based therapy remain unresolved. Here, we show that inducing tumor-cell ferroptosis enhances anti-tumor immunity by potentiating major histocompatibility complex II (MHC-II)-dependent antigen presentation in tumor-infiltrating macrophages. Multi-omics analyses reveal that all-trans retinoic acid (ATRA) released from ferroptotic tumor cells directly targets CD38 through the transcriptional factor retinoic acid receptor alpha (RARα) and activates transcription factor EB (TFEB) to control MHC-II expression in macrophage by inducing autophagy. Clinically, a ferroptosis signature correlates with improved immunotherapy response. We also developed a drug-free nano-redox lever that selectively targets and disrupts glutathione metabolism in hypoxic tumor regions by accepting electrons, thereby potentiating ferroptosis-mediated immune stimulation. This creates a positive feedback loop wherein activated macrophages further promote immune-driven tumor ferroptosis, synergizing with anti-PD-1 (programmed cell death protein 1) therapy across preclinical models. Together, our study identifies an uncovered role for ferroptosis in tumor immunity and provides a clinically translatable approach to enhance immunotherapy efficacy. - Source: PubMed
Publication date: 2026/04/29
Sun Jia-LeiChu Yong-ChaoWang FuYu Ding-DangLiu Jin-RuiXu Ru-ChenLiu Hua-HuaQi Zhuo-RanShi XuanYu Xiang-NanYao Yi-KunLiu Tao-TaoWeng Shu-QiangDong LingShen Xi-ZhongHu Shi-BinSun TaoZhu Ji-Min