IKK_beta Recombinant Adenovirus
- Known as:
- IKK_beta Recombinant Adenovirus
- Catalog number:
- ADV-305
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Cell Biolabs
- Gene target:
- IKK_beta Recombinant Adenovirus
Related products to: IKK_beta Recombinant Adenovirus
Related articles to: IKK_beta Recombinant Adenovirus
- Obesity is heterogeneous, and personalising management requires stratifiers beyond BMI. In Chinese populations, the Phlegm‑Dampness Constitution (PDC) is a clinically defined traditional medicine phenotype consistently overrepresented among adults with obesity, yet its molecular characterisation remains incomplete. - Source: PubMed
Publication date: 2026/08/25
Hu QingZhang ZhenzhenLi XingmingJiang HanminLiu JingyiRong ChenxiChen Huimin - West Nile virus (WNV) is a mosquito-borne pathogen of escalating epidemiological importance and a growing global health concern, driven by the climate-associated expansion of its mosquito vectors. Although WNV is an extensively studied flavivirus, most host-pathogen interaction studies focus on static and structural aspects rather than dynamic and functional ones. Delineating phosphorylation-mediated interactions between WNV proteins and human kinases bridges a critical gap by providing important insight into the molecular mechanisms underlying infection. In this study, we investigated potential phosphorylation-mediated interactions between WNV proteins and human kinases using an integrative computational framework combining motif prediction, phosphoproteomic data analysis and structural docking. Key interactions were predicted between viral proteins and regulatory kinases within the AKT-ERK pathway and the AMPK-mediated autophagy, including major network kinases such as RAF1, IKBKB, and ULK1. In addition, experimentally validated phosphorylation sites in viral proteins were found to be associated with multiple candidate host kinases, including MAP2K7 and MAP2K9, suggesting complex regulatory networks. Integration with phosphoproteomic datasets supported the relevance of multiple predicted kinases, including those associated with antiviral responses and translational regulation. Protein-protein docking demonstrated stable, energetically favorable interactions between selected host kinases and viral proteins, particularly the viral polymerase (NS5), helicase (NS3), and NS1. The findings of this study establish a framework for future research on the development of host-directed antiviral strategies. - Source: PubMed
Publication date: 2026/07/27
Anil AkashJabbar Ayisha AShaji VineethaAhmed MukhtarJoseph Bristow BenAjayakumar Aromal MonipillilModi Prashant KumarJayanandan AbhithajSoman SowmyaSubbannayya YashwanthRaju Rajesh - Caspase-8 and the NF-κB essential modulator (NEMO, also referred to as IKKγ) play critical roles in controlling TNF-α-induced cell death and survival in hepatocytes. The aim of this study was to generate a hepatocyte-derived cell line in which the and genes can be conditionally inactivated simultaneously to investigate the significance of the corresponding signaling pathways. To this end, we induced hepatocellular carcinoma in mice using diethylnitrosamine and established an immortalized hepatoma cell line from explanted liver tumors, which is subsequently referred to as ΔCN60. ΔCN60 cells still retain floxed and alleles, allowing for efficient Cre-mediated deletion to generate derivatives. Loss of both Caspase-8 and NEMO inhibits cell proliferation, increases the expression of tumor and progenitor markers (AFP, CD133), reduces albumin expression, and blocks TNF-α-induced NF-κB p65 nuclear translocation. ΔCN60 cells display altered sensitivity to prolonged TNF-α exposure, suggesting a potential shift in necroptosis-associated signaling pathways, although necroptotic cell death was not directly demonstrated. ΔCN60 serves as a versatile hepatoma model for investigating Caspase-8/NEMO-dependent TNF-α signaling and hepatocyte plasticity and may help prioritize future in vivo experiments by enabling selected mechanistic questions to be addressed first in vitro. - Source: PubMed
Publication date: 2026/07/24
Cornejo Müller AlejandroLiehr ThomasBalakrishnan PrahladKankel StefanieBuhl Eva MKeller Diandra THardt Katharina SSchröder-Lange Sarah KLiedtke ChristianWeiskirchen Ralf - Inflammation causes bone loss by dysregulating the differentiation and functions of osteoclasts, osteoblasts, and osteocytes. This process can be modeled by the expression of constitutively activated IKK2 (IKK2ca), a strategy that we leveraged to investigate the mechanisms through which inflammation negatively affects cells of the osteoblast/osteocyte lineage. We found that mice expressing IKK2ca in osteoblasts exhibit significant bone loss. Mechanistically, IKK2ca downregulates the expression of osteoblast genes while inducing the differentiation of bone-forming osteoblasts into catabolic osteocytes like cells, expressing high levels of Podoplanin, Fgf23, Dkk1 and Sclerostin. We term these atypical inflammatory osteocyte-like cells (aiOCy-L cells) as they highly express inflammatory and senescence markers and promote osteoclast differentiation as well. Additional data show that inflammation induces abnormal differentiation of OB into aiOCy-L cells through upregulating mTOR and glycolysis. In summary, we uncovered a mechanism by which inflammation alters osteoblast differentiation and fate decision via the IKK2/mTOR/glycolysis axis. - Source: PubMed
Publication date: 2026/08/04
Swarnkar GauravAhmad Md FahimZeyad MarwaTyagi Abdul MalikNaaz MusarratMbalaviele GabrielAbu-Amer Yousef - Non-small cell lung cancer (NSCLC) is the predominant subtype of lung malignancy. Accumulating epidemiological evidence demonstrates that environmental lead (Pb) exposure as a critical driver of its initiation and progression. - Source: PubMed
Publication date: 2026/07/30
Xu YinlanDong JieLiu HejunZheng JinmeiGuo HaonanChen YueWang JialinWu Weidong