CHUK Antibody
- Known as:
- CHUK Antibody
- Catalog number:
- XW-7281
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CHUK Antibody
Related genes to: CHUK Antibody
- Gene:
- CHUK NIH gene
- Name:
- component of inhibitor of nuclear factor kappa B kinase complex
- Previous symbol:
- TCF16
- Synonyms:
- IKK1, IKK-alpha, IkBKA, NFKBIKA, IKKA
- Chromosome:
- 10q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-15
- Date modifiied:
- 2019-02-21
Related products to: CHUK Antibody
Related articles to: CHUK Antibody
- Approximately 20-40% of patients with diabetes mellitus (DM) develop diabetic kidney disease (DKD), a major microvascular complication of the condition. This study aimed to explore the potential diagnostic value of hsa-miR-5585-3p for DKD, and its regulatory effects, by targeting CHUK, on inflammatory factor expression and NLRP3 activation in HK-2 cells induced by high glucose (HG). - Source: PubMed
Publication date: 2026/05/14
Zeng JingQin XuexiangWang JielianXiong CunyouFeng Xiaoyun - IκB kinase alpha (IKKα) is a central regulator of non-canonical NF-κB signalling and contributes modestly to canonical NF-κB signalling, both of which mediate well-established aspects of immune function and inflammation. Emerging evidence now indicates that IKKα also performs a wide range of atypical functions, influencing NF-κB indirectly or acting through mechanisms independent of either NF-κB pathway. Several IKKα substrates have been identified outwith these classical signalling routes, and a recently described truncated isoform, p45-IKKα, has further expanded its known roles. This review examines how IKKα, through these diverse signalling modalities, contributes to disease processes including inflammatory disorders and cancer. Particular attention is given to both NF-κB-dependent and NF-κB-independent mechanisms that shape disease development, tumor biology, and ageing. Recent studies have also linked IKKα gene variants (CHUK) to altered IKKα function and patient outcomes, and advances in medicinal chemistry combined with early pharmacological testing have produced the first selective inhibitors of this kinase. Together, this review provides an updated and integrated overview of the complex biology of IKKα and its emerging potential as a therapeutic target. - Source: PubMed
Publication date: 2026/05/10
Tinto KirstyCunningham MargaretPlevin Robin - Antimicrobial resistance (AMR) in , and ., known as ESKAPE pathogens, continue to pose a health threat globally. In Rwanda, data on long-term trends and resistance profiles among these pathogens remain limited. This study has assessed the temporal trends in the distribution and AMR patterns of ESKAPE pathogens at the University Teaching Hospital of Kigali (CHUK) from 2020 to 2024. - Source: PubMed
Publication date: 2026/04/23
Uwamariya MartheDushimirimana TheophileAkayezu DenyseMukanyandwi AngeliqueMusana Muhire Francois RegisMutsaka-Makuvaza Masceline JenipherTuyisenge LisineNyundo MartinMpunga TharcisseMunyemana Jean Bosco - ATG16L1 (autophagy related 16 like 1) is a core macroautophagy/autophagy protein essential for autophagosome formation. It also functions in non-canonical autophagy pathways such as LC3-associated phagocytosis (LAP) and in other processes including immunity, inflammation, and membrane trafficking. This review synthesizes recent advances and proposes that ATG16L1 functions as a central molecular integrator governed by a multi-layered regulatory code. This framework includes genetic polymorphisms, transcriptional control, and diverse post-transcriptional and post-translational mechanisms. We detail how these regulatory layers collectively fine-tune ATG16L1 function in response to cellular stress. Dysregulation of this network contributes broadly to human diseases including inflammatory bowel disease, cancer, and neurodegenerative disorders. Notably, the functional impact of specific regulatory events is highly context dependent, a principle exemplified by the Crohn disease-associated T300A polymorphism. Deciphering this regulatory landscape and its crosstalk with both autophagy-dependent and autophagy-independent functions positions ATG16L1 as a pivotal node in cellular homeostasis and as an emerging therapeutic target. ATG: autophagy related; CASM: conjugation of Atg8-family proteins to single membranes; CCD: coiled-coil domain; CEBPA/CEBPα: CCAAT enhancer binding protein alpha; CHUK/IKKA: component of inhibitor of nuclear factor kappa B kinase complex; circRNA: circular RNA; CPT1A: carnitine palmitoyltransferase 1A; CREB: cAMP responsive element binding protein; CSNK2: casein kinase 2; FTO: FTO alpha-ketoglutarate dependent dioxygenase; GJA8/connexin 50: gap junction protein alpha 8; H/R: hypoxia-reoxygenation; HDAC: histone deacetylase; KAT2B/PCAF: lysine acetyltransferase 2B; KDM1A: lysine demethylase 1A; LAP: LC3-associated phagocytosis; lncRNA: long non-coding RNA; LRRK2: leucine rich repeat kinase 2; mA: N6-methyladenosine; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; miRNA/MIR: microRNA; Mtb: ; ncRNA: non-coding RNA; PE: phosphatidylethanolamine; PI3K: phosphoinositide 3-kinase; PRKA/PKA: protein kinase cAMP-activated; PPP1: protein phosphatase 1; RAB33B: RAB33B, member RAS oncogene family; RB1CC1/FIP200: RB1 inducible coiled-coil 1; SETD7: SET domain containing 7, histone lysine methyltransferase; SQSTM1/p62: sequestosome 1; TNF/TNF-α: tumor necrosis factor; ULK: unc-51 like autophagy activating kinase; V-ATPase: vacuolar-type H-translocating ATPase; VDR: vitamin D receptor; WIPI2B: WD repeat domain, phosphoinositide interacting 2B; YTHDF2: YTH N6-methyladenosine RNA binding protein F2; ZDHHC7: zDHHC palmitoyltransferase 7. - Source: PubMed
Publication date: 2026/05/14
Wei FujingLiu ZhenzhenYu XiaoyingSun YinqiZhao YuanyuanWang YuFeng ZilingZhao XiaozhuKe XiaoxueYang AiminCui Hongjuan - Depression is a significant global health issue characterized by complex underlying mechanisms. This study aimed to investigate the role of cholinergic neuron-specific heat shock protein 60 (HSP60) in modulating lipopolysaccharide (LPS)-induced neuroinflammation and depressive-like behaviours in mice. Cholinergic neuron-specific HSP60 knockout mice were generated by crossing Hsp60-flox mice with Chat-cre mice. Genotyping confirmed the successful creation of the knockout. The effects of LPS on weight loss, behavioural changes, cytokine levels, neuroinflammation markers and signalling pathway proteins were assessed. Behavioural assessments included the tail suspension test and sucrose preference test. HSP60 knockout mice exhibited mitigated weight loss in response to LPS. Behavioural tests indicated that HSP60 deficiency alleviated LPS-mediated depressive-like behaviours without affecting locomotor activity. In the hippocampus, LPS treatment significantly altered cytokine levels, increasing pro-inflammatory cytokines at the same time as decreasing anti-inflammatory cytokines. HSP60 knockout mice partially reversed these effects, showing increased anti-inflammatory and decreased pro-inflammatory cytokines. LPS-induced upregulation of neuroinflammation markers such as glial fibrillary acidic protein, NLRP3 (i.e. NOD-, LRR- and pyrin domain-containing protein 3) and p-IKKα/β [i.e. the phosphorylated forms of the catalytic subunits of the IκB kinase (IKK) complex, specifically IKKα (CHUK) and IKKβ] was significantly reduced in HSP60 knockout mice. Additionally, LPS-induced elevation of phosphorylated eukaryotic translation initiation factor 2α levels in the hippocampus was attenuated by HSP60 deficiency, without affecting other signalling pathway proteins. These findings suggest that HSP60 in cholinergic neurons plays a critical role in regulating LPS-induced neuroinflammation and depressive-like behaviours. Targeting HSP60 in cholinergic neurons may provide a therapeutic approach for mitigating neuroinflammation and associated depressive symptoms. KEY POINTS: Specific knockout of HSP60 in cholinergic neurons could protect against LPS-induced physiological and behavioral impairments, including mitigated weight loss, improved depressive-like behaviors, and unaffected locomotor activity. Cholinergic neuron-specific HSP60 deletion could attenuate neuroinflammation by reversing LPS-induced cytokine imbalance, suppressing key inflammatory markers (GFAP, NLRP3, cGAS, p-IKKα/β), and crucially, by preserving hippocampal acetylcholine levels, a key neurotransmitter with established anti-inflammatory properties. HSP60 deficiency selectively reduces the LPS-induced phosphorylation of the eukaryotic translation initiation factor 2α (p-eIF2α) in the hippocampus, indicating a targeted modulation of the cellular stress and protein synthesis regulation pathway, without altering other major signaling molecules. - Source: PubMed
Publication date: 2026/05/07
Wei XiangzanZhong XiaoniOuyang YuLiu YongxiangQin Weirong