Ask about this productRelated genes to: GZMB antibody
- Gene:
- GZMB NIH gene
- Name:
- granzyme B
- Previous symbol:
- CTLA1, CSPB
- Synonyms:
- CCPI, CGL-1, CSP-B, CGL1, CTSGL1, HLP, SECT
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-12
- Date modifiied:
- 2016-10-05
Related products to: GZMB antibody
Related articles to: GZMB antibody
- Cancer remains a major public health challenge worldwide. Tumor reprogramming has emerged as a novel therapeutic strategy for cancer treatment. However, despite increasing interest in this approach, whether tumor cells can be stably and efficiently reprogrammed into cytotoxic effector cells remains unclear. Here, we engineered multiple types of tumor cells to overexpress T cell effectors including IFNG, FASLG, or PRF1/GZMB and evaluated their cytotoxic potential. We found that tumor cells engineered to overexpress these genes can inhibit cell autonomous proliferation in vitro. Co-culture assays showed that overexpression of IFNG or FASLG enabled tumor cells to kill neighboring tumor cells, whereas PRF1/GZMB overexpression had no such effect. However, the cytotoxic effect mediated by IFNG overexpression was much stronger than that mediated by FASLG overexpression. Moreover, IFNG overexpressing tumor cells suppressed the growth of wild-type tumor cells without evident toxicity in vivo. These findings establish a potent strategy for reprogramming tumor cells to acquire tumor-killing activity and suggest a potential new direction for cancer therapies. - Source: PubMed
Publication date: 2026/05/14
Li HaoyangZhu YunfeiHao YanHu QinlinMa QiongqiongLi JiarongSun YangyangHou YintingZhang RuixingHong ZhangyongLiang HuabinFu XueliZhang Hongru - NK cells are the core cells of the innate immune system, which can kill cancer cells non-specifically and almost do not cause immune rejection or neurotoxicity, thereby enabling broad application in immune cell therapy. The KLRG1/Cadherin signaling axis has been reported to inhibit the anti-tumor response of NK cells. However, the mechanism by which KLRG1 regulates CAR NK cell function remains unclear. - Source: PubMed
Publication date: 2026/05/14
Chen YiranFarooq Muhammad AsadHui XinhuiHuang YunheHu YueXue MinAjmal IqraRen YaojunJi YuzhouWang ChenJiang Wenzheng - Alopecia areata (AA) is an autoimmune hair-loss disorder driven by aberrant T-cell activation and immune-epithelial crosstalk. To identify actionable upstream regulators, we established a proteome-anchored multi-omics framework integrating genetic instruments, lesional transcriptomics, and single-cell immune profiling. - Source: PubMed
Publication date: 2026/03/11
Pan LingfengLi CaihongYang Liehao - Responses to atezolizumab plus bevacizumab (Atezo+Bev) in hepatocellular carcinoma (HCC) are heterogeneous, and response determinants remain unclear. We investigated whether spatial proximity between PD-L1(+) tumor-associated macrophages (TAMs) and CD8(+) T cells represents an immune niche associated with Atezo+Bev responsiveness. - Source: PubMed
Publication date: 2026/04/29
Nosaka TakutoOhtani MasahiroYamashita JunkiMurata YosukeAkazawa YuTanaka TomokoTakahashi KazutoNaito TatsushiImamura YoshiakiKoneri KenjiGoi TakanoriNakamoto Yasunari - Vesicular cutaneous lupus erythematosus (VCLE) is a rare autoimmune disease in dogs and is considered the canine counterpart of human subacute cutaneous lupus erythematosus (SCLE). However, the molecular mechanisms underlying VCLE remain incompletely defined. - Source: PubMed
Publication date: 2026/05/11
Keating TreasaStranahan LaurenWiener DominiqueKeating M KellyLeon RenatoBanovic Frane