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
- Smoking cessation decreases lung cancer progression; however, its effects on precancerous lesions and the underlying mechanisms remain unclear. This study established a mouse model of precancerous pulmonary nodules and employed single-cell RNA sequencing (scRNA-seq) and immune repertoire sequencing (IR-seq) to elucidate the regulatory mechanisms by which smoking cessation influences the development of lung precancerous lesions. - Source: PubMed
Publication date: 2026/08/13
Wang XintongTang FangQin JiayuXiao TiquanShi LiweiZhang ShujunChe Chunli - This study aimed to identify and prioritize gut microbiota-derived metabolite-associated host candidate targets in high-risk primary biliary cholangitis (PBC) through integrative multi-omics analysis and external validation. - Source: PubMed
Publication date: 2026/08/13
Feng JingLiu ZhiyunSun Huanna - Following acute kidney injury (AKI), a substantial subset of patients experiences an irreversible progression to chronic kidney disease (CKD), yet the molecular determinants governing this maladaptive transition remain elusive, and effective clinical interventions are lacking. Here, we identify lactate as a key metabolic determinant orchestrating the transition from AKI to CKD. Analysis of the UK Biobank cohort reveals that elevated circulating lactate independently predicts CKD development in AKI patients and correlates with fibrotic progression. Using murine ischemia-reperfusion injury models, we demonstrate that lactate drives sustained renal damage through post-translational lactylation of the RNA helicase DDX18. Mechanistically, p300-mediated lactylation of DDX18 at lysine 116 disrupts its nucleolar retention, causing redistribution to the nucleoplasm where it acquires enhanced binding affinity for CD44 mRNA. This subcellular relocalization stabilizes CD44 mRNA through altered RNA-protein interactions, thereby amplifying fibrotic signaling pathways. Therapeutically, we developed a kidney-targeted, cell-penetrating peptide that specifically inhibits DDX18 K116 lactylation, effectively attenuating fibrotic progression in injured kidneys. Our findings establish protein lactylation as a regulatory mechanism governing RNA helicase nucleolar localization and subsequent control of mRNA stability, revealing a potential therapeutic target for interrupting fibrotic processes in chronic kidney disease. - Source: PubMed
Publication date: 2026/08/13
Dong LijunXie JingwenTao MengyuanLiu ShuaiLu YueyangWu TianxingGeng JianChen QingyunZhao XiaoshanZhao JianboZhou JiaHou HonghaoAi JunTao TaoZuo Daming - Cancer immunotherapy has transformed cancer treatment, yet its efficacy remains limited by a "cold" tumor immune microenvironment (TIME) characterized by poor T cell infiltration. Induction of immunogenic cell death (ICD) improves T cell infiltration by promoting the release of T-cell-recruiting chemokines such as CXCL10. However, the outcome may be limited by dipeptidyl peptidase IV (DPP4), a serine protease that degrades CXCL10 and related chemokines. We report that chemotherapeutic agents, particularly those capable of inducing strong ICD, transcriptionally upregulate DPP4 in cancer cells, establishing a negative feedback mechanism that dampens CXCL10-mediated immune responses. To overcome this limitation, we developed an enhanced triple-combination immunochemotherapy based on the codelivery of doxorubicin, a DPP4 inhibitor (Sitagliptin, Sitag), and a COX-2 inhibitor (5-ASA) using a 5-ASA-derivatized hyaluronic acid (HA) dendrimer nanocarrier (HASA). HA is a natural ligand for CD44 that is overexpressed on tumor and tumor endothelial cells, enabling precise targeting. In preclinical tumor models, this strategy enhanced T cell infiltration, antitumor immunity, and therapeutic efficacy while minimizing systemic toxicity, resulting in significant survival benefit when combined with anti-PD-1 therapy. Our work identifies chemotherapy-induced DPP4 upregulation as an adaptive immune-resistance feedback loop and establishes a targeted triple-drug nanoplatform that integrates chemotherapy, DPP4 inhibition, and COX-pathway modulation for enhanced immunochemotherapy. - Source: PubMed
Publication date: 2026/08/04
Chen ShangyuLi ShichenLuo ZhangyiHuang YixianZhang HuaMu YiqingZhang BeiChen Chien-YuHou GanqianZhang MinLi Song - Intrahepatic cholangiocarcinoma (ICC) is an aggressive malignancy with poor prognosis and limited treatment options. Disulfidptosis, a novel cell death pathway driven by disulfide bond accumulation, has emerged as a potential mechanism in cancer biology; however, its role in ICC remains unclear. - Source: PubMed
Publication date: 2026/07/29
Qiao WanjiaHe YixiangLi JingLiu XiaohanZhang LingfangBai XinWang YeyingTang Jianming