ADCK5
- Known as:
- ADCK5
- Catalog number:
- 001190A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADCK5
Related genes to: ADCK5
- Gene:
- ADCK5 NIH gene
- Name:
- aarF domain containing kinase 5
- Previous symbol:
- -
- Synonyms:
- FLJ35454
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-21
- Date modifiied:
- 2016-04-25
Related products to: ADCK5
Related articles to: ADCK5
- Lactobacillus rhamnosus (LGG) can alleviate ovalbumin (OVA)-induced asthma, but whether its mechanism of action involves cell senescence is unknown. OVA was used to establish a mouse model of asthma. LGG was administered by oral gavage, and a lentivirus carrying aarF domain containing kinase 5 (ADCK5) was injected intravenously to overexpress ADCK5. The Penh value of the airway response in the mice was measured by a whole-body plethysmography system. Airway epithelial cell senescence was assessed using an SA-β-gal kit, immunofluorescence, and Western blotting. DCFH-DA, ELISA, a JC-1 fluorescent probe, a transmission electron microscope, immunofluorescence, and Kwik-Diff staining were used to evaluate oxidative stress and the inflammatory response in the lung tissue of the mice. Finally, the expression of the ADCK5/PI3K/AKT axis was detected by Western blotting. LGG improved AHR levels in OVA-induced asthmatic mice; alleviated inflammatory infiltration, tube wall thickening, goblet cell hyperplasia, and collagen deposition in lung tissues; and reduced the number of SA-β-gal-positive cells and P21 and P16 expression. LGG can reduce ROS and γH2AX levels, increase MMP levels, improve mitochondrial structural damage, and reduce the levels of inflammatory factors in BALF and the IgE concentration in serum. LGG also reduced ADCK5, p-PI3K, and p-AKT levels. ADCK5 overexpression increased the number of SA-β-gal-positive cells and the P21, P16, p-PI3K, p-AKT, ROS, and γH2AX levels; decreased the MMP; and increased the inflammatory factor and IgE concentrations. LGG may reduce oxidative stress and the inflammatory response potentially through inhibiting the ADCK5/PI3K/AKT axis, improving airway epithelial cell senescence, and thus alleviating asthma. - Source: PubMed
Publication date: 2025/11/12
Zhu PeiqinYang TongYe HantingTan LiWang JunyangYang ZihanMao Wei - Severe asthma poses a significant challenge in clinical management due to its poor responsiveness to conventional therapies and worse overall prognosis. Identifying differentially expressed genes (DEGs) between severe asthma and non-severe asthma, exploring potential therapeutic targets, and intervening in these targets could offer new strategies to overcome the treatment bottleneck in severe asthma and improve clinical outcomes. Bioinformatics analysis first revealed that DEGs between severe and non-severe asthma were predominantly enriched in the longevity-regulating pathway, which is closely linked to cellular senescence. Subsequent in vitro experiments confirmed a heightened level of cellular senescence in severe asthma. Notably, ADCK5 was identified as a highly expressed senescence-related marker in severe asthma, exhibiting both strong predictive value for the condition and a clear association with cellular senescence. Finally, through high-throughput compound screening, molecular docking, and experimental validation, Leucokinin VIII acetate (Leucokinin 8) was found to inhibit ADCK5 expression and reduce excessive cellular senescence. In summary, ADCK5 emerges as a critical gene involved in airway senescence in severe asthma, and Leucokinin 8 may offer therapeutic potential by targeting ADCK5 to alleviate airway senescence, thus improving severe asthma outcomes. - Source: PubMed
Publication date: 2025/08/29
Feng LingZhong YuanLi LiZhang MingzhenZhu ManniWang JiayueHuang MaoJi NingfeiMa Yuan - AarF domain-containing kinases (ADCKs) are a family of putative mitochondrial proteins that have been implicated in various aspects of mitochondrial function and cellular metabolism. Mitochondria play a crucial role in cellular bioenergetics, primarily in adenosine triphosphate (ATP) production, while also regulating metabolism, thermogenesis, apoptosis, and reactive oxygen species (ROS) generation. Evidence suggests that the ADCK family of proteins is involved in maintaining mitochondrial architecture and homeostasis. In detail, these proteins are believed to play a role in processes such as coenzyme Q biosynthesis, energy production, and cellular metabolism. There are five known isoforms of ADCK (ADCK1-ADCK5), some of which have similar activities, and each also has its own unique biological functions. Dysregulation or mutations in specific ADCK isoforms have been linked to several pathological conditions, including multiple human cancers, primary coenzyme Q10 (CoQ10) deficiency, and metabolic disorders. This review surveys the current body of peer-reviewed research on the ADCK protein family, incorporating data from the primary literature, case studies, and experimental studies conducted in both in vitro and in vivo systems. It also draws on existing review articles and known published findings to provide a comprehensive overview of the functional roles, disease associations, and molecular mechanisms of ADCK proteins. Further in-depth research on ADCK proteins has the potential to unlock critical insights into their precise mechanisms. This could pave the way for identifying new therapeutic targets for mitochondrial and metabolic-related diseases, as well as for advancing cancer treatment strategies. - Source: PubMed
Publication date: 2025/06/17
Jacquet NoelZhao Yunfeng - The bromodomain and extraterminal (BET) family of proteins show altered expression across various cancers. The members of the bromodomain (BRD) family contain epigenetic reader domains that bind to acetylated lysine residues in both histone and non-histone proteins. Since BRD proteins are involved in cancer initiation and progression, therapeutic targeting of these proteins has recently been an area of interest. In experimental settings, JQ1, a commonly used BRD inhibitor, is the first known inhibitor to target BRD-containing protein 4 (BRD4), a ubiquitously expressed BRD and extraterminal family protein. BRD4 is necessary for a normal cell cycle, and its aberrant expression activates pro-inflammatory cytokines, leading to tumor initiation and progression. Various BRD4 inhibitors have been developed recently and tested in preclinical settings and are now in clinical trials. However, as with many targeted therapies, BRD inhibitor treatment can lead to resistance to treatment. Here, we investigated the kinases up-regulated on JQ1 treatment that may serve as target for combination therapy along with BRD inhibitors. To identify kinase targets, we performed a comparative analysis of gene expression data using RNA from BRD inhibitor-treated cells or BRD-modulated cells and identified overexpression of several kinases, including FYN, NEK9, and ADCK5. We further validated, by immunoblotting, the overexpression of FYN tyrosine kinase; NEK9 serine/threonine kinase and ADCK5, an atypical kinase, to confirm their overexpression after BRD inhibitor treatment. Importantly, our studies show that targeting FYN or NEK9 along with BRD inhibitor effectively reduces proliferation of cancer cells. Therefore, our research emphasizes a potential approach of utilizing inhibitors targeting some of the overexpressed kinases in conjunction with BRD inhibitors to enhance therapeutic effectiveness. - Source: PubMed
Publication date: 2024/09/05
Chandrashekar Darshan SAfaq FarrukhKarthikeyan Santhosh KumarAthar MohammadShrestha SadeepSingh RajeshManne UpenderVarambally Sooryanarayana - The mechanism of mitochondria-related genes (MRGs) in childhood allergic asthma (CAS) was unclear. The aim of this study was to find new biomarkers related to MRGs in CAS. - Source: PubMed
Publication date: 2024/05/23
Zhao WeiFang HongjuanWang TaoYao Chao