NF-κB inducing kinase: a key regulator in the immune system and in cancer.

Cytokine Growth Factor Rev

Department of Veterans Affairs Medical Center, Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.

Published: August 2010

NF-κB inducing kinase (NIK) is a kinase that activates the canonical and non-canonical NF-κB pathways to control transcriptional expression of certain proteins such as cytokines, chemokines and NF-κB signaling molecules. Many advances have been made in understanding the molecular mechanisms by which the stability of NIK is regulated to affect downstream signaling. Genetic mouse models suggest that NIK plays an essential role in the regulation of the immune system as well as in the bone microenvironment. Increasing evidence links NIK to the tumorigenesis of hematological cancers, such as multiple myeloma, and solid tumors, such as pancreatic carcinoma and melanoma. Understanding the mechanism by which NIK is de-regulated will potentially provide therapeutic options for certain diseases such as autoimmunity and cancer.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2939163PMC
http://dx.doi.org/10.1016/j.cytogfr.2010.06.002DOI Listing

Publication Analysis

Top Keywords

nf-κb inducing
8
inducing kinase
8
immune system
8
nik
5
nf-κb
4
kinase key
4
key regulator
4
regulator immune
4
system cancer
4
cancer nf-κb
4

Similar Publications

Neurotransmitter release is triggered in microseconds by the two C domains of the Ca sensor synaptotagmin-1 and by SNARE complexes, which form four-helix bundles that bridge the vesicle and plasma membranes. The synaptotagmin-1 CB domain binds to the SNARE complex via a 'primary interface', but the mechanism that couples Ca-sensing to membrane fusion is unknown. Widespread models postulate that the synaptotagmin-1 Ca-binding loops accelerate membrane fusion by inducing membrane curvature, perturbing lipid bilayers or helping bridge the membranes, but these models do not seem compatible with SNARE binding through the primary interface, which orients the Ca-binding loops away from the fusion site.

View Article and Find Full Text PDF

Structural Transformation and Degradation of Cu Oxide Nanocatalysts during Electrochemical CO Reduction.

J Am Chem Soc

January 2025

Liquid Sunlight Alliance, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, California 94720, United States.

The electrochemical CO reduction reaction (CORR) holds enormous potential as a carbon-neutral route to the sustainable production of fuels and platform chemicals. The durability for long-term operation is currently inadequate for commercialization, however, and the underlying deactivation process remains elusive. A fundamental understanding of the degradation mechanism of electrocatalysts, which can dictate the overall device performance, is needed.

View Article and Find Full Text PDF

Background: Nitrous oxide (N₂O), commonly known as laughing gas, is widely recognized for its anesthetic and analgesic effects, and is frequently used in medical contexts. However, its misuse can lead to significant neurological complications, which are often under-recognized in clinical practice. Recent data on such cases in Germany are rare.

View Article and Find Full Text PDF

Bi-targeting of thioredoxin 1 and telomerase by thiotert promotes cell death of myelodysplastic syndromes and lymphoma.

Biol Direct

January 2025

Department of Clinical Laboratory, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, Zhejiang, China.

Thioredoxin1 (TRX1) and telomerase are both attractive oncology targets that are tightly implicated in tumor initiation and development. Here, we reported that the 6-dithio-2-deoxyguanosine analog thiotert exhibits an effective cytotoxic effect on myelodysplastic syndromes (MDS) cell SKM-1 and lymphoma cell U-937. Further studies confirmed that thiotert effectively disrupts cellular redox homeostasis, as evidenced by elevated intracellular reactive oxygen species (ROS) levels, increased MnSOD, accelerated DNA impairment, and activated apoptosis signal.

View Article and Find Full Text PDF

Tangeretin alleviates sepsis-induced acute lung injury by inhibiting ferroptosis of macrophage via Nrf2 signaling pathway.

Chin Med

January 2025

Department of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, 1665 Kongjiang Road, Shanghai, 200092, China.

Background: Sepsis-induced acute lung injury (ALI) is a severe clinical condition accompanied with high mortality. Tangeretin, which is widely found in citrus fruits, has been reported to exert antioxidant and anti-inflammatory properties. However, whether tangeretin protects against sepsis-induced ALI and the potential mechanisms remain unclear.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!