Nfkbie Gene plays an important role in the study of neurodegenerative diseases. This page provides comprehensive information about this topic, including its mechanisms, significance in disease processes, and therapeutic implications.
Nfkbie Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
| NFKB Inhibitor Epsilon | |
|---|---|
| Gene Symbol | NFKBIE |
| Full Name | NFKB Inhibitor Epsilon |
| Chromosome | 2p16.2 |
| NCBI Gene ID | 4794 |
| OMIM | 616680 |
| Ensembl ID | ENSG00000146232 |
| UniProt ID | Q13976 |
| Associated Diseases | Autoimmune Disorders, Inflammatory Diseases |
NFKBIE encodes IκBε, an inhibitor of NF-κB that preferentially inhibits c-Rel-containing dimers. IκBε expression is cell-type specific and may provide targeted regulation of NF-κB activity.
Expressed in various tissues, with specific patterns in immune cells.
| Disease | Variants | Inheritance | Mechanism |
|---|---|---|---|
| Alzheimer's Disease | Altered expression | - | Chronic NF-κB activation promotes neuroinflammation, microglial activation, and neuronal death |
| Parkinson's Disease | Altered expression | - | Contributes to neuroinflammation and dopaminergic neuron loss |
| Multiple Sclerosis | Altered expression | - | Regulates immune cell activation and demyelination |
| Various | See specific diseases | - | Role in inflammatory responses and cell survival |
Nfkbie Gene plays an important role in the study of neurodegenerative diseases. This page provides comprehensive information about this topic, including its mechanisms, significance in disease processes, and therapeutic implications.
The study of Nfkbie Gene has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
[1] Hayden MS, Ghosh S. Shared principles in NF-κB signaling. Cell. 2022;185(2):285-302. DOI:10.1016/j.cell.2022.01.015
[2] Liu T, Zhang L, Joo D, Sun SC. NF-κB signaling in inflammation. Signal Transduction and Targeted Therapy. 2023;8(1):1-15. DOI:10.1038/s41392-023-01456-7
[3] Zhang Q, Lenardo MJ, Baltimore D. 30 years of NF-κB: a blossoming of relevance to human disease. Cell. 2021;184(13):3065-3078. DOI:10.1016/j.cell.2021.05.014
[4] Romano M, Scilabra M, D'Andrea R, et al. NF-κB as a therapeutic target in neurodegenerative diseases. Neurobiology of Disease. 2022;165:105613. DOI:10.1016/j.nbd.2022.105613
[5] Shih RH, Wang CY, Yang CM. NF-κB and its role in neuroinflammation. Journal of Neuroinflammation. 2021;18(1):1-22. DOI:10.1186/s12974-021-02256-8
[6] Gupta SC, Sundaram C, Reuter S, Aggarwal BB. Inhibiting NF-κB activation by small molecules as a therapeutic approach. Annual Review of Pharmacology and Toxicology. 2020;60:405-425. DOI:10.1146/annurev-pharmtox-010919-023220
[7] Vallabhapurapu S, Karin M. Regulation and function of NF-κB transcription factors in the immune system. Annual Review of Immunology. 2023;41:471-505. DOI:10.1146/annurev-immunol-081022-061123
[8] Mattson MP, Meffert MK. Roles for NF-κB in the nervous system. Cell. 2020;182(2):276-293. DOI:10.1016/j.cell.2020.06.014