OTUD6B Human Protein
- Known as:
- OTUD6B Human Protein
- Catalog number:
- 80407
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- BPS Bioscience
- Gene target:
- OTUD6B Human Protein
Related genes to: OTUD6B Human Protein
- Gene:
- OTUD6B NIH gene
- Name:
- OTU domain containing 6B
- Previous symbol:
- -
- Synonyms:
- CGI-77, DUBA5
- Chromosome:
- 8q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-28
- Date modifiied:
- 2014-11-18
Related products to: OTUD6B Human Protein
Related articles to: OTUD6B Human Protein
- To investigate the functional role of OTU deubiquitinase 6B-antisense transcript 1 (OTUD6B-AS1) and its potential association with parthanatos - a poly (ADP-ribose) polymerase 1 (PARP-1)/apoptosis-inducing factor (AIF)-mediated regulated cell death pathway - in esophageal adenocarcinoma (EAC), which remains poorly understood. - Source: PubMed
Publication date: 2026/07/15
Zheng QingfengWu QiuliLin YulingChen Xiangbo - Triple-negative breast cancer (TNBC) is a clinically challenging disease subtype of breast cancer, with therapeutic outcomes remaining unsatisfactory due to its highly invasive potential. Ferroptosis, a newly identified type of programmed cell death, is mediated by the iron-dependent accumulation of lipid peroxides, presenting a potential therapeutic avenue for the treatment of TNBC. Calycosin (Cal) has demonstrated antitumor effects across various tumors; however, its therapeutic potential based on the ferroptosis pathway for TNBC treatment and the associated mechanisms remains unclear. - Source: PubMed
Publication date: 2026/07/08
Mao XueLin YinGu ZhifengZhang Erhao - - Source: PubMed
Publication date: 2026/05/19
Yang DianLiu YichaoHong YueshunMiao EnmingWang PengSun YumingZhou LinaLiu ShuyanZhang YingqiuQin HongqiangYe MingliangLiu Han - The mechanism underlying acute pancreatitis (AP) is not fully understood. And the effect of s-adenosylhomocysteine hydrolase-like protein 1 (AHCYL1) in AP is unknown. - Source: PubMed
Publication date: 2026/05/09
Xiao JuanLi WanlianPan JianYang YinhuiChen Ji-AoLong Xi-Dai - Hepatocellular carcinoma (HCC) treatment faces dual challenges: resistance to targeted therapy and low response rates to immunotherapy. These issues are rooted in the immunosuppressive tumor microenvironment (TME). Ferroptosis and autophagy, two critical cellular processes, play complex and paradoxical roles in HCC drug resistance and immunoregulation, and they interact closely. This review explores how the OTU deubiquitinase family, especially OTUB1, acts as a central hub coordinating the autophagy-ferroptosis balance. Additionally, other OTU family members, such as OTUD3, OTULIN, and OTUD6B, contribute to HCC progression by modulating similar pathways, highlighting the need for a broader therapeutic approach. Specifically, OTUD3 suppresses HIF-1α-driven angiogenesis, OTULIN inhibits NF-κB-mediated inflammation, and OTUD6B stabilizes pVHL to impede metastasis, collectively demonstrating their synergistic or antagonistic interactions with OTUB1 in reshaping the TME. This coordination drives HCC drug resistance and remodels the immune microenvironment. OTUB1 suppresses ferroptosis and maintains tumor cell survival by deubiquitinating and stabilizing key proteins like SLC7A11, GPX4, and p62. It also promotes immune escape by modulating PD-L1 stability and immune cell function. Consequently, therapeutic strategies targeting the OTU family-such as developing selective inhibitors for multiple members, using intelligent nanodelivery systems, and combining them with ferroptosis inducers or immune checkpoint inhibitors-show significant potential for reversing drug resistance and improving immunotherapy efficacy. Expanding these strategies to include other OTU members could enhance efficacy and reduce resistance. Addressing how the OTU family precisely modulates the intersection of autophagy and ferroptosis, and how it reshapes immune cell metabolism and function within the TME, is critical for developing novel combination therapies. This article provides a crucial theoretical foundation for developing novel combination strategies targeting metabolism-immune crosstalk. - Source: PubMed
Publication date: 2026/05/05
Zhao PengchengZhang Ping