CTLA_4
- Known as:
- CTLA_4
- Catalog number:
- ANT-116
- Product Quantity:
- 500µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- CTLA_4
Related genes to: CTLA_4
- Gene:
- CTLA4 NIH gene
- Name:
- cytotoxic T-lymphocyte associated protein 4
- Previous symbol:
- CELIAC3, IDDM12
- Synonyms:
- CD152, CD, GSE, CTLA-4
- Chromosome:
- 2q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2019-04-23
Related products to: CTLA_4
Activation B7-1 antigen,B7,BB1,CD28LG,CD28LG1,CD80,CTLA-4 counter-receptor B7.1,Homo sapiens,Human,LAB7,T-lymphocyte activation antigen CD80Anti-CTLA-4 produced in goat AntibodyAnti-Human CD152 (CTLA-4) Biotin 100 ugAnti-Human CD152 (CTLA-4) Functional Grade Purified 100 ugAnti-Human CD152 (CTLA-4) PE 100 testsAnti-Human CD152 (CTLA-4) PE 100 testsAnti-Human CD152 (CTLA-4) PE 25 testsAnti-Human CD152 (CTLA-4) PE 25 testsAnti-Human CD152 (CTLA-4) Purified 100 ugAnti-Human CD152 (CTLA-4) Purified 25 ugAnti-human CTLA-4_CD152 Monoclonal AntibodyAnti-Mouse CD152 (CTLA-4) APC 100 ugAnti-Mouse CD152 (CTLA-4) APC 25 ugAnti-Mouse CD152 (CTLA-4) Biotin 100 ugAnti-Mouse CD152 (CTLA-4) Biotin 50 ug Related articles to: CTLA_4
- Evidence on serious infection (SI)-risk with advanced therapies across immune-mediated inflammatory diseases (IMIDs) is limited. We compared SI- and sepsis-rates within a global-IMID network and assessed whether these are consistent across IMIDs. - Source: PubMed
Publication date: 2026/09/23
Allen VictoriaGibson MarkAdas MaryamChavali RohanDe Gracia LeighHussain HassanMuzafar ImanMuzafar SamaadSuresh NithyaYoon YoungsungBechman KatieBrown JeremyRussell MarkGoodman Anna LLangan Sinead MNorton SamPhillippo DavidWelton NickyGalloway James - The mechanisms that cause hypertension remain elusive despite more than a century of investigation. Some of its triggers include aging, sex, salt, diet, stress, experience with adversity, socio-cultural-economic disparities, and poor-quality sleep. The renin-angiotensin-aldosterone and the endothelin systems and other hormones contribute to varying degrees to the rise in BP and target organ damage. It has become increasingly recognized that inflammation and the innate and adaptive immune systems play a role in the etiopathogenesis of hypertension. We review here the participation of different cellular and molecular (genetic and epigenetic) mechanisms that play a role in hypertension via the immune system, including neutrophil extracellular traps, memory T cells, and aldosterone-modulated trained immunity mediated by monocytes/macrophages. Molecular mechanisms, including the effects of neutrophil gelatinase-associated lipocalin as an immunomodulator, and the role of isolevoglandins in mediating oxidative stress-induced activation of the adaptive immune system are analysed. We conclude by summarizing potential therapeutic avenues to address inflammation in hypertension. - Source: PubMed
Publication date: 2026/09/18
Fields EviatarBerillo OlgaSchiffrin Ernesto L - MicroRNAs (miRNAs) are small non-coding RNAs that have emerged as critical regulators of gene expression and key cellular processes in cancer, including tumor cell proliferation, survival, metastasis, and both innate and adaptive immune responses within the tumor microenvironment. Through their ability to modulate immune cell development, differentiation, polarization, antigen presentation, cytokine signaling and immune checkpoint expression, miRNAs play a vital role in shaping immune responses and represent attractive therapeutic candidates for remodeling the tumor immune microenvironment. This review provides a comprehensive overview of the mechanisms through which miRNAs regulate anti-tumor immunity and contribute to immune evasion with particular emphasis on their role in modulating major immune checkpoint pathways, including PD-1/PD-L1, CTLA-4, LAG-3, TIM-3 and CD28-mediated signaling. We further examine the contribution of miRNAs to therapeutic resistance and discuss their potential integration with immune checkpoint blockade, chemotherapy, PARP inhibitors and targeted therapies to enhance antitumor efficacy and overcome treatment resistance. Recent advances in spatial transcriptomics and computational approaches have expanded our understanding of miRNA-mediated regulatory networks at single-cell and tissue levels and provide new insights into tumor-immune interactions. In addition, we evaluate the current progress in the clinical development of miRNA-based therapeutics, including miRNA mimics and inhibitors and discuss the major challenges associated with efficient delivery, off-target effects, immunogenicity and patient heterogeneity. Collectively, the evidence highlights the growing potential of miRNAs as diagnostic biomarkers, therapeutic targets and therapeutic tools in cancer immunotherapy. Continued advances in RNA therapeutics, delivery technologies and multi-omics approaches are expected to accelerate the clinical translation of miRNA-based strategies for personalized cancer therapy. - Source: PubMed
Publication date: 2026/09/01
Biltekin EzgiOzpolat Bulent - Cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) exists not only as a membrane-bound immune checkpoint but also as a naturally secreted soluble isoform (sCTLA-4), generated primarily through exon 3 skipping. This review focuses specifically on splice-derived sCTLA-4 and examines its biological and clinical significance. sCTLA-4 is shaped by immune state, cellular source, and tissue microenvironment. Mechanistically, sCTLA-4 can restrain B7/CD28-dependent immune activation, while recent preclinical evidence suggests a preferential effect on type 1 immune responses. In autoimmune and inflammatory diseases, longitudinal changes in sCTLA-4 often parallel changes in immune activity, although its performance as a disease-specific biomarker remains limited. In cancer, associations with tumor burden, prognosis, and treatment response are more variable and appear to depend strongly on the surrounding immune context. Thus, circulating sCTLA-4 may be better viewed as a state-dependent immunoregulatory signal than as a universal standalone biomarker. Current evidence does not clearly establish whether its elevation is causal, compensatory, or epiphenomenal. Key translational priorities include detection methods that distinguish sCTLA-4 isoforms and cellular sources, standardized longitudinal sampling, biomarker panels that integrate sCTLA-4 with defined immune phenotypes, and therapeutic strategies tailored to specific immune contexts while preserving peripheral tolerance. - Source: PubMed
Publication date: 2026/09/08
Cai XueYu LihuaLiu XiaoliJiang TingtingLi JunxiangYang Zhiyun - Immunotherapy has reshaped the adjuvant landscape, with several immune checkpoint inhibitors (ICIs) approved in different tumor types. This meta-analysis evaluates the benefit of adjuvant ICIs across solid tumors. - Source: PubMed
Publication date: 2026/09/07
Polito Mariam GraziaSisca LuisanaCaruso DavideCosimati AntonellaRamirez Reinaga Carla AdrianaLeka EtienSantini DanieleSpinelli Gian Paolo