BAK1 Antibody
- Known as:
- BAK1 Antibody
- Catalog number:
- 32009
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- BAK1 Antibody
Related genes to: BAK1 Antibody
- Gene:
- BAK1 NIH gene
- Name:
- BCL2 antagonist/killer 1
- Previous symbol:
- CDN1
- Synonyms:
- BCL2L7, BAK
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-09
- Date modifiied:
- 2016-02-24
Related products to: BAK1 Antibody
Related articles to: BAK1 Antibody
- The innate immune signaling pathway cGAS-STING plays an important role in the recognition of cytosolic nucleic acids and the induction of the interferon-dependent antiviral response. Despite the significant research interest in this cascade in the context of immune system function, the mechanisms regulating cGAS-STING signaling and the switch between its pro-inflammatory and pro-apoptotic effects remain largely underexplored. According to publicly available RNA-seq data and microarray analyses, SETD7 lysine methyltransferase participates in interferon signaling in cancer cells. This study aims to elucidate the role of SETD7 in the regulation of the STING-dependent immune response in human lung adenocarcinoma (LUAD) cells. For this purpose, we developed a reproducible and cost-effective method for inducing the STING cascade by transfecting cells with salmon sperm DNA (sspDNA). We demonstrated that sspDNA efficiently induces phosphorylation of the key components of the STING-TBK1-IRF3 signaling pathway and activates the expression of interferons and pro-inflammatory cytokines. Using this approach, we further demonstrated that SETD7 is involved in the regulation of the IRF3-dependent transcriptional program. Suppression of SETD7 was associated with changes in the expression of genes related to innate immune response and apoptosis, including increased levels of , , , (PUMA), and . Furthermore, attenuation of SETD7 expression reduced the lentiviral transduction efficacy in H1299 cells. These results suggest that SETD7 may play a role in regulating the switch in STING signaling between pro-inflammatory and pro-apoptotic responses in LUAD cells. - Source: PubMed
Publication date: 2026/04/30
Nevzorov Ivan AKorableva PolinaShuvalov OlegParfenyev SergeyBarlev Nickolai ADaks Alexandra - Acute myeloid leukemia (AML) is a complex blood cancer that primarily affects relapsing or refractory patients receiving conventional chemotherapy. Nonsteroidal anti-inflammatory drugs (NSAIDs) have anticancer properties with restricted clinical efficacy attributable to cyclooxygenase (COX)-induced toxicities. To address this issue, a group of benzylamide analogs of the classical NSAIDs (NSI-1-NSI-9) were developed and synthesized to mask the carboxylic acid moiety and minimize COX-induced adverse effects while maintaining anticancer activity. The cytotoxic effect of such substances has been demonstrated in some leukemia cell lines (HL-60, MV4-11, KG1a, and K562). NSI-5 exerted the highest anti-leukemic activity among these sulindac analogs, as determined at a sub-micromolar level in all cell lines studied, by IC50. This mechanistic data also demonstrated that NSI-5 induced apoptosis that was dose-dependent, especially in HL-60 cell lines, and increased the sub-G1 cell fraction. This apoptotic process was also accompanied by a significant decrease in mitochondrial membrane potential, which is characteristic of the induction of the intrinsic apoptotic process. Interestingly, NSI-5 decreased the intracellular reactive oxygen species (ROS) and the expression of most antioxidants (catalase and glutathione synthetase), as well as the redox balance. Gene characterization in vitro also suggested activation of apoptotic pathways, where expression of , , and increased, suggesting a potential p53-independent apoptotic pathway, in contrast to control for expression. Collectively, these findings indicate that NSI-5 is a promising in vitro anti-leukemic lead compound, with activity associated with mitochondrial dysfunction and altered redox regulation. The observed effects are consistent with previously reported COX-independent activity of structurally related NSAID derivatives, and support further investigation of NSI-5 in preclinical models. - Source: PubMed
Publication date: 2026/04/26
Alkhatabi Hind ABasabrain MohammedAlahmadi Alaa GAlzahrani Shiekhah MMuhammad Yosra AAlmuhaiyawi MahaAlreemi Maha MAlotibi Reem MAlreemi Roaa MAlkhattabi Heba AHassan Reem NAl-Bishri Wedad MEl-Mezgueldi MohammedOmar Abdelsattar M - Lip and oral cavity cancers are among the most common types of cancer worldwide and remain a major health problem due to poor prognosis and treatment- related side effects. Therefore, identifying new naturally derived compounds with selective cytotoxic effects on oral cancer cells is essential. Vulpinic acid, a lichenderived secondary metabolite, has shown antioxidant and anticancer activities in various cancer types. However, its effects on oral cancer cells have not yet been clarified. This study aims to investigate the cytotoxic and apoptotic effects of vulpinic acid on oral cancer cells and to explore its possible molecular mechanisms. - Source: PubMed
Publication date: 2026/05/04
Şengüm Dilara NurAlkan Ayşe HaleBozkurt Fatma ZeynepMutlu PelinCansaran-Duman Demet - Bacterial quorum sensing (QS) signals an increasing threat during pathogenesis. How plants deploy timely defenses through QS perception is poorly understood. Here, we report that perceives 2'-aminoacetophenone (2'-AA), a volatile QS signal from , and mounts a multilayered defense. This response comprises BRI1-ASSOCIATED RECEPTOR KINASE 1 (BAK1)-dependent intracellular immunity, extracellular quorum quenching through the release of acetic acid, and ecological remodeling of the root microbiome to suppress . Our findings demonstrate that plants can translate the detection of a specific bacterial QS molecule into a coordinated, preemptive disease resistance strategy. - Source: PubMed
Publication date: 2026/04/28
He DanxiaZhou YangLi MengWang MiaoYu WenjiaShao ChuyangSingh Sunil KumarGu MeijiaoWang YuhuaYuan JianlongWu XiaoxuanZheng ShuaiXie YiChen LixianMorcillo Rafael J LYang YuVílchez Juan IgnacioZhang Jin-LinMiao YansongMacho Alberto PZhang Huiming - Liver cancer is one of the most prevalent and lethal cancers worldwide, characterized by poor prognosis and limited treatment options. Triptophenolide (TRI), a diterpenoid compound, has shown anti-proliferative activity in breast and pancreatic cancers, but its role in liver cancer remains largely unexplored. In this study, TRI significantly inhibited the proliferation of HepG2 (hepatoblastoma) and HuH7 (hepatocellular carcinoma) cells in a dose-dependent manner, with IC values decreasing from 279.9 to 229.4 µg/mL (24-48 h) in HepG2 and from 441.1 to 282.6 µg/mL in HuH7. Colony formation assays confirmed the suppression of HCC cell growth. TRI also promoted apoptosis, increasing apoptotic rates to 68.99% in HepG2 and 43.34% in HuH7 at 400 µg/mL (48 h). Cell cycle analysis revealed S-phase arrest, with TRI raising the S-phase population to 42.02% and 45.38%, respectively. Mechanistically, TRI upregulated pro-apoptotic genes (, //, , , , ) and proteins, activating the mitochondrial apoptotic pathway. In vivo, TRI (10 mg/kg) markedly reduced tumor volumes in HepG2 and HuH7 xenografts compared with controls, without obvious systemic toxicity. These findings suggest that TRI exerts anti-proliferative, pro-apoptotic, and cell cycle regulatory effects in HCC. However, further preclinical studies are warranted to elucidate its mechanisms and evaluate its safety profile. - Source: PubMed
Publication date: 2026/04/03
Sabeel ZufaChen RuolanLiu YanChen XiaoyangZhang WenjingPan ShangyangYing LuYu ChangyuanYang Zhao