Monoclonal anti_human BAK1 antibody (AT8B4)
- Known as:
- Monoclonal anti_human BAK1 (anti-) (AT8B4)
- Catalog number:
- ATGA0183
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- Monoclonal anti_human BAK1 antibody (AT8B4)
Related genes to: Monoclonal anti_human BAK1 antibody (AT8B4)
- 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: Monoclonal anti_human BAK1 antibody (AT8B4)
Related articles to: Monoclonal anti_human BAK1 antibody (AT8B4)
- -based probiotics are increasingly recognized for their potential to enhance intestinal health in companion animals, yet their mechanisms of action in canine epithelial systems remain incompletely defined. This study aimed to evaluate whether a live probiotic consortia (BC) modulates epithelial barrier integrity, immune signaling, apoptosis-renewal pathways, and metabolic activity in canine-relevant intestinal and macrophage cell models. MCA-B1 proximal gastrointestinal epithelial cells and DH82 macrophage-like cells were exposed to BC cultures, followed by quantification of tight-junction expression, permeability (FITC-Dextran), cytokine responses, phagocytic activity, apoptosis-related markers, and metabolomic profiles. BC treatment significantly strengthened the epithelial barrier, inducing a marked upregulation of Claudin 1 (CLDN1) (11.3 fold), CLDN4 (2.4 fold), Occludin (OCLN, 1.7 fold), and increasing key proteins including ZO-2 and cingulin while reducing LPS-induced FITC-Dextran permeability to 94.5%. BC concurrently modulated innate immune signaling, increasing MyD88 (33.2%), IL-8 (14.6 fold), IL-18 (2.6 fold), and IFNB1 protein levels, while enhancing anti-inflammatory regulation, including a robust rise in DH82-derived IL-10. Apoptosis-renewal markers shifted toward physiological turnover, with increased BCL2 (1.9 fold) and reduced BAK1. Metabolomic profiling of BC activity revealed elevated AMP, abundant Peptide Transporter 1 (PEPT1)-transportable peptides, increased γ-glutamyl metabolites, and lower Glutathione disulfide (GSSG), consistent with AMPK-linked tight-junction assembly and glutathione-supported redox buffering. Together, these data indicate that -derived metabolites positively influence barrier-related, immunological, and metabolic responses in a canine proximal intestinal epithelial system and modulate functional responses in macrophage-like cells. These in vitro findings contribute to the mechanistic understanding of host cellular responses to -associated metabolites. - Source: PubMed
Publication date: 2026/05/15
Udrea Andreea CorneliaLarsen Katrine BieRekima AkilaSchwarzenberg AdrianBak Steffen YdeChristensen NielsShen Chong - The wall-associated kinases (WAKs) and WAK-like proteins (WAKLs) comprise a unique receptor-like kinase subfamily in plants, which have been shown to regulate plant development and defense responses by sensing cell wall-derived components, such as pectin or pectin fragments. In this study, we aimed to characterize the function of in flg22-triggered immunity in . Through functional analyses of genes in , we identified as the most pronouncedly induced member in response to flg22 treatment. Gain- and loss-of-function genetic analyses were performed to assess its role in flg22-triggered immune responses, including mitogen-activated protein kinase (MAPK) activation, reactive oxygen species (ROS) burst, and defense gene induction. Transgenic plants expressing a kinase domain-deleted mutant () were generated. Co-immunoprecipitation assays were conducted to examine interactions with FLAGELLIN-SENSITIVE 2 (FLS2) and BRI1-ASSOCIATED RECEPTOR KINASE 1 (BAK1). Heterologous overexpression of in tomato was also tested for bacterial disease resistance. positively regulates flg22-triggered immune responses. Interestingly, retains the capacity to potentiate these responses. Co-immunoprecipitation assays showed that both wild-type WAKL10 and WAKL10-ΔK constitutively associate with FLS2 and BAK1. Overexpression of in tomato confers enhanced bacterial disease resistance. The extracellular domain of WAKL10 promotes FLS2-BAK1 complex formation, thereby contributing to flg22 signaling. This study reveals a new function of WAKLs, distinguished from their proposed role in sensing cell wall components. The functional conservation of WAKL10 suggests its potential application in engineering disease resistance in crop plants. - Source: PubMed
Publication date: 2026/05/09
Zhang LuGao JialeYao LingyaHe Yunxia - To investigate the role of peroxiredoxin isoforms (Prdx) in the radioresistance of cancer cells, the expression of Prdx1-6, DNA repair genes, and apoptosis regulators was studied in human cancer cell lines with varying radiosensitivities (A549, Caco-2, and MCF-7) after exposure to ionizing radiation. A correlation was found between high constitutive Prdx1-6 expression levels and increased radioresistance. Predominantly cytosolic isoforms Prdx2 and Prdx6 demonstrated pronounced induction after irradiation, indicating their critical role in protecting against radiation-induced oxidative stress. Most radiosensitive A549 cells exhibited the lowest baseline Prdx expression and the most pronounced transcriptional changes after irradiation, whereas MCF-7 and Caco-2 cells had higher constitutive expression and a weaker response to radiation. Mitochondrial Prdx3 and Prdx5, as well as ER-localized Prdx4, exhibited relatively stable expression. A549 cells demonstrated the highest induction of DNA repair genes, which may indicate more severe DNA damage. In contrast, MCF-7 cells were characterized by high basal expression of repair genes and elevated γH2AX levels before irradiation, which may reflect their "readiness" for repair and explain their higher radioresistance. Furthermore, radioresistant MCF-7 cells had increased expression of anti-apoptotic genes (BCL2, MCL1, BIRC5), suppressing the mitochondrial apoptotic pathway. Meanwhile, A549 cells showed higher induction of pro-apoptotic genes (PUMA, NOXA, BAK1) and activation of caspase-3, which correlates with their increased radiosensitivity. Therefore, peroxiredoxins protect cells from radiation exposure, either by being constitutively expressed or by being highly inducible in response to radiation, and promote cell survival after irradiation. This makes them attractive targets for overcoming cancer cell radioresistance. - Source: PubMed
Publication date: 2026/05/27
Sharapov M GGoncharov R GKarmanova E EParfenyuk S BGlushkova O VLunin S M - 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