Ask about this productRelated genes to: CD44 antibody
- Gene:
- CD44 NIH gene
- Name:
- CD44 molecule (Indian blood group)
- Previous symbol:
- MIC4, MDU2, MDU3
- Synonyms:
- IN, MC56, Pgp1, CD44R, HCELL, CSPG8
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
Related products to: CD44 antibody
Related articles to: CD44 antibody
- Breast cancer remains one of the most prevalent malignancies among women worldwide, and despite advances in therapy and treatment options, tumour relapse and metastasis remain major clinical challenges, largely driven by the breast cancer stem cells (BCSCs) niche that resists conventional treatments and regenerates tumours. In breast cancer, where approximately 30% of patients who initially respond to treatment ultimately relapse and die of metastatic disease, targeting BCSCs is critical for improving patient outcomes. Cyclin-dependent kinase inhibitor 1A/p21 (CDKN1A/p21) is a multifunctional protein that is known primarily for its role in regulating the cell cycle in response to DNA damage. However, in this study, we aimed to explore the role of CDKN1A/p21 in the survival and expansion of BCSCs. - Source: PubMed
Publication date: 2026/04/22
Manousakis EvangelosMoreta-Moraleda CristinaMiralles Clàudia MartinezTomàs Pujolà AnnaBaccara HoudaFranquet Laia LiñánMontañés Albó MontserratFerrari RobertoWright Roni H G - Durable CD4 T cell memory is essential against mycobacterial infection, yet activation-induced cell death (AICD) limits the survival of activated clones after BCG vaccination. The upstream, cell-intrinsic brakes that govern this bottleneck remain incompletely defined. Combining transcriptomics, loss-of-function tests, and engineering, we identify as a pro-apoptotic regulator that is downregulated in memory CD4 T cells and promotes activation-induced death in T cell models. We develop an activation-gated AAV platform in which an NFAT-IL-2 promoter drives Cre to flip a FLEXed U6-shRNA cassette, and package them into a single AIO vector. This design confines silencing to antigen-experienced T cells, preferentially within the CD4CD44 compartment. In BCG-vaccinated mice, transient activation-linked inhibition expands CD4 T cells, enhances IL-2 and Th1-skewed recall responses, lowers pulmonary, and splenic bacterial burdens after challenge. These findings highlight a strategy to selectively modulate intrinsic death pathways during immune priming for strengthening vaccine-elicited T cell memory. - Source: PubMed
Publication date: 2026/04/03
Liu ZixuanLiu WeihuangZhao ChenyuBai XuanchangZhou FangtingSun HangShi JiaheChen PinruLiu MinPan Qin - Dermatomyositis (DM) is an immune-mediated myopathy marked by chronic inflammation and heterogeneous clinical trajectories. The molecular determinants driving disease onset and progression remain poorly defined. This study aimed to construct a high-accuracy diagnostic risk model, identify causally relevant genes, and uncover cell-type-specific immune circuits contributing to DM pathogenesis, with emphasis on BTN3A2. - Source: PubMed
Publication date: 2026/04/30
Yang JingYin Long-KuanTang Jin - Hypoxia, glutathione (GSH) overexpression, and lactate accumulation within the solid tumor microenvironment severely constrain the efficacy of photocatalytic therapy. Here, we report a CD44-targeted cascade nanoplatform (CNMLH) constructed via layer-by-layer assembly to remodel this metabolic barrier. The platform features a hollow graphitic carbon nitride (CN) core, sequentially coated with an in situ grown MnO shell, an electrostatically adsorbed lactate oxidase (LOx) layer, and an outermost hyaluronic acid (HA) coating. Upon HA-mediated internalization, the outer coating degrades to release LOx, which selectively consumes lactate to produce HO. Subsequently, the exposed MnO shell scavenges endogenous GSH and converts the generated HO into O. This catalytic cascade effectively disrupts the tumor's antioxidant defense system and alleviates local hypoxia. Consequently, under subsequent light irradiation, the CN core overcomes the hypoxic restriction to efficiently generate reactive oxygen species (ROS), thereby triggering robust immunogenic cell death (ICD). Both in vitro and in vivo experimental results confirm that this metabolism-intervening strategy effectively reverses the immunosuppressive microenvironment while eliciting antitumor immune responses. - Source: PubMed
Publication date: 2026/04/30
Ma Xiang-YuPan TingJin Xiao-KangZhang Shi-ManZeng XuanZhang Xian-Zheng - Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that occupies a central regulatory position within pulmonary immune networks, integrating inflammatory signalling, redox control, and immune-stromal communication. Originally characterised as a pro-inflammatory mediator, MIF is now recognised to exert context-dependent functions ranging from protective host defence during acute infection to the promotion of chronic inflammation, fibrosis, and tumour progression. This review synthesises current evidence on the molecular biology and signalling mechanisms governing MIF activity in the lung, highlighting its role as a network hub coordinating CD74/CD44- and CXCR-mediated signalling, glucocorticoid antagonism, and redox imbalance. A systems biology perspective illustrates how genetic variability, environmental exposure, ageing, and metabolic stress reprogram MIF-centred immune circuits across pulmonary diseases. Integration of multi-omics and computational modelling identifies opportunities for selective modulation of MIF signalling. Disease-specific roles in pneumonia, COPD, fibrosis, and lung cancer are discussed, positioning MIF as a key immunoregulatory node for future therapeutic strategies. - Source: PubMed
Aygun AliyarbayovaYaqut HajiyevaSara PashayevaGuney QaniyevaSevda QarayevaArzu Mekhtiyeva