Target Name: KCNK16
NCBI ID: G83795
Review Report on KCNK16 Target / Biomarker Content of Review Report on KCNK16 Target / Biomarker
KCNK16
Other Name(s): potassium channel, subfamily K, member 16 | Potassium channel subfamily K member 16 | Potassium two pore domain channel subfamily K member 16, transcript variant 3 | OTTHUMP00000223326 | pancreatic potassium channel Talk-1 | MGC133123 | Potassium channel, subfamily K, member 16 | TWIK-related alkaline pH-activated K(+) channel 1 | KCNK16 variant 3 | TALK-1 | KCNK16 variant 2 | 2P domain potassium channel Talk-1 | Potassium channel subfamily K member 16 (isoform 3) | potassium channel, two pore domain subfamily K, member 16 | OTTHUMP00000223327 | K2p16.1 | Potassium channel, two pore domain subfamily K, member 16 | KCNKG_HUMAN | Pancreatic potassium channel Talk-1 | TALK1 | BIK | Potassium two pore domain channel subfamily K member 16, transcript variant 2 | potassium two pore domain channel subfamily K member 16 | Potassium channel subfamily K member 16 (isoform 2) | OTTHUMP00000223328 | OTTHUMP00000223325 | OTTHUMP00000016345

Regulation of KCNK16 Activity By Drugs

KCNK16 is a protein that is expressed in various tissues of the body, including the brain, heart, and skeletal muscles. It is a member of the subfamily K of the potassium channel family and its function is to regulate the intracellular potassium levels. KCNK16 plays a crucial role in the regulation of muscle contractions, which is essential for movement and maintaining posture.

Diseases and Abnormalities

KCNK16 is implicated in various diseases and abnormalities, including epilepsy, heart failure, and muscle weakness. In epilepsy, KCNK16 is known to play a negative role in the regulation of neuronal excitability and has been shown to be involved in the pathophysiology of epilepsy. Studies have shown that modulating the activity of KCNK16 can be a potential therapeutic approach for the treatment of epilepsy.

In heart failure, KCNK16 is expressed in the cardiac muscle and is involved in the regulation of the contractions of the heart. The loss of function of KCNK16 has been implicated in the development and progression of heart failure. Therefore, modulating the activity of KCNK16 has has been shown to be a potential therapeutic approach for the treatment of heart failure.

In muscle weakness, KCNK16 is involved in the regulation of muscle contractions and has been implicated in the development and progression of muscle weakness. The loss of function of KCNK16 has been shown to contribute to muscle weakness and the loss of muscle mass in older adults. Therefore, modulating the activity of KCNK16 has been shown to be a potential therapeutic approach for the treatment of muscle weakness.

Chemical Modulation

Several chemical modifications of KCNK16 have been identified, including phosphorylation, acetylation, and polyglutamylation. These modifications play important roles in the regulation of the activity of KCNK16 and are potential drug targets.

Phosphorylation of KCNK16 has been shown to play a negative role in the regulation of neuronal excitability and is therefore a potential drug target. Studies have shown that modulating the activity of KCNK16 by phosphorylation can be a potential therapeutic approach for the treatment of epilepsy and other neurological disorders.

Acetylation of KCNK16 has been shown to play a positive role in the regulation of neuronal excitability and is therefore a potential drug target. Studies have shown that modulating the activity of KCNK16 by acetylation can be a potential therapeutic approach for the treatment of epilepsy and other neurological disorders.

Polyglutamylation of KCNK16 has been shown to play a negative role in the regulation of neuronal excitability and is therefore a potential drug target. Studies have shown that modulating the activity of KCNK16 by polyglutamylation can be a therapeutic potential approach for the treatment of epilepsy and other neurological disorders.

Drugs that Modulate KCNK16 Activity

Several drugs have been shown to modulate the activity of KCNK16 and have been identified as potential therapeutic approaches for various diseases.

One class of drugs that have been shown to modulate the activity of KCNK16 is the channel blockers. These drugs work by blocking the channels through which KCNK16 is expressed and have been shown to be effective in modulating the activity of KCNK16. channel blockers such as amikacin , auromodulin, and cinnamopurine have been shown to be effective in modulating the activity of KCNK16 and have been shown to be potential therapeutic approaches for the treatment of epilepsy.

Another class of drugs that have been shown to modulate the activity of KCNK16 are the kinases. These drugs work by activating the activity of GCa+ channels, which are involved in the regulation of neuronal excitability. drugs such as

Protein Name: Potassium Two Pore Domain Channel Subfamily K Member 16

Functions: Outward rectifying potassium channel. Produces rapidly activating and non-inactivating outward rectifier K(+) currents

The "KCNK16 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about KCNK16 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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KCNK17 | KCNK18 | KCNK2 | KCNK3 | KCNK4 | KCNK5 | KCNK6 | KCNK7 | KCNK9 | KCNMA1 | KCNMB1 | KCNMB2 | KCNMB2-AS1 | KCNMB3 | KCNMB4 | KCNN1 | KCNN2 | KCNN3 | KCNN4 | KCNQ Channels (K(v) 7) | KCNQ1 | KCNQ1DN | KCNQ1OT1 | KCNQ2 | KCNQ3 | KCNQ4 | KCNQ5 | KCNQ5-AS1 | KCNQ5-IT1 | KCNRG | KCNS1 | KCNS2 | KCNS3 | KCNT1 | KCNT2 | KCNU1 | KCNV1 | KCNV2 | KCP | KCTD1 | KCTD10 | KCTD11 | KCTD12 | KCTD13 | KCTD13-DT | KCTD14 | KCTD15 | KCTD16 | KCTD17 | KCTD18 | KCTD19 | KCTD2 | KCTD20 | KCTD21 | KCTD21-AS1 | KCTD3 | KCTD4 | KCTD5 | KCTD5P1 | KCTD6 | KCTD7 | KCTD8 | KCTD9 | KDELR1 | KDELR2 | KDELR3 | KDF1 | KDM1A | KDM1B | KDM2A | KDM2B | KDM3A | KDM3B | KDM4A | KDM4B | KDM4C | KDM4D | KDM4E | KDM5A | KDM5A-GATAD1-EMSY chromatin complex | KDM5B | KDM5C | KDM5D | KDM6A | KDM6B | KDM7A | KDM7A-DT | KDM8 | KDR | KDSR | KEAP1 | Kelch-like protein | KERA | Keratin | KHDC1 | KHDC1L | KHDC1P1 | KHDC3L | KHDC4 | KHDRBS1