User:Gloryrunner13/sandbox
Appearance
- Summary (Function)
- Localized in dendrites and cell body (1)
- Mediator of apoptosis in hippocampal, cortical and granule neurons (1)
- Apoptosis function induced by increase in reactive oxygen species (ROS)
- Structure
- Functional Alpha Subunit (4), (8)
- All K+ channels have a pore of alpha-subunits; one to two copies of a conserved loop P-domain
- P-domain contains selectivity sequence allowing only K+ ions, and only those of a certain class (“functional diversity of families”)
- Associate with auxiliary cytoplasmic beta subunits
- 2 types: 6TM spanning regions, 2TM regions
- 6TM: conserved gene families: Kv, KCNQ, EAG-like, and Ca activated
- 2TM: inward rectifying
- Large number of phosphorylation sites (1)
- Functional Alpha Subunit (4), (8)
- Regulation
- Expression is developmentally regulated (1)
- Poorly conducting in phosphorylated state (1)
- Blockers
- Selectivity
- Stromatoxin- voltage-clamp experiments; low selectivity (2)
- Hanatoxin- inhibits K+ voltage gated channel activation (2)
- Guangxitoxin-1E- high selectivity for Kv2 channels (2)
- Selectivity
- Kinetics
- Repolarization
- N- and C-terminal regions are main factors in activation kinetics of this channel. (3) (5)
- Channelopathies/Mutations
- Epileptic Encephalopathy (6)
- Developmental Disabilities
- Deficiencies in: neurotransmitter regulation, heart rate, insulin production, hearing, etc.
- Developmental Disabilities
- Epileptic Encephalopathy (6)
- Physiological Roles in Diseases
- Neurodegenerative Diseases: Oxidative modulation of K2.1 channels contributes to altered excitability, progression of neurodegenerative diseases, and healthy aging. (7)
- Diabetes (Pancreatic Bcell Signaling) : K(+) efflux mediated by KV2.1 delayed rectifier K(+) channels acts as a brake for insulin secretion. (9) (10)
- Alzheimers: Injury-mediated increased K(+) efflux through Kv2.1 channels promotes neuronal apoptosis, contributing to widespread neuronal loss in neurodegenerative disorders such as Alzheimer's disease. (11)
- Pharmocology
- Anti-apoptotic strategy (1)
- CO can protect against an increase in KCNC1 current by regulating ROS and PKG
- Cancer cells and chronic viruses produce excess CO
- CO can protect against an increase in KCNC1 current by regulating ROS and PKG
- Anti-apoptotic strategy (1)
References
- http://www.wjgnet.com/1949-8454/full/v5/i2/85.htm
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972724/
- https://www.ncbi.nlm.nih.gov/pubmed/14608450
- https://www.ncbi.nlm.nih.gov/pubmed/12451110
- https://www.ncbi.nlm.nih.gov/pubmed/18607586
- http://www.pcmicroscopycore.com/the-jordyn-project-kcbn1
- https://www.ncbi.nlm.nih.gov/pubmed/25333910
- https://www.ebi.ac.uk/interpro/entry/IPR005400
- https://www.ncbi.nlm.nih.gov/pubmed/25052376
- https://www.ncbi.nlm.nih.gov/pubmed/20711225
- https://www.ncbi.nlm.nih.gov/pubmed/24323720
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