SLC22A6: A Potential Drug Target for Diabetes, Alzheimer's and Parkinson's Diseases

Target Name: SLC22A6

NCBI ID: G9356

SLC22A6

SLC22A6: A Potential Drug Target for Diabetes, Alzheimer's and Parkinson's Diseases

SLC22A6 (MGC45260) is a protein that is expressed in various tissues of the body, including the brain, heart, and liver. It is a member of the SLC family of transport proteins, which are responsible for transporting a variety of molecules across the cell membrane. SLC22A6 is specifically involved in the transport of glucose across the blood-brain barrier, which is a critical function for maintaining the brain's energy supply.

SLC22A6 is a potential drug target for several diseases, including diabetes, Alzheimer's disease, and Parkinson's disease. These conditions are characterized by the progressive loss of brain cells, which can lead to a range of symptoms, including cognitive decline, behavior changes, and loss of function.

One of the key challenges in developing new treatments for these conditions is identifying the underlying causes and mechanisms. SLC22A6 is a well-established player in the regulation of glucose transport, and its dysfunction has been implicated in the development and progression of several neurological conditions.

SLC22A6 is a transmembrane protein that consists of an intracellular N-terminal region, a catalytic region, and an extracellular C-terminal region. It is expressed in a variety of tissues, including the brain, heart, and liver, and is involved in the transport of glucose across the blood-brain barrier.

SLC22A6 is a member of the SLC family of transport proteins, which are responsible for transporting a variety of molecules across the cell membrane. It is specifically involved in the transport of glucose across the blood-brain barrier, which is a critical function for maintaining the brain's energy supply.

SLC22A6 functions as a Glucose Transporter

SLC22A6 is a glucose transporter, which means it is responsible for transporting glucose across the blood-brain barrier. The blood-brain barrier is a specialized barrier that separates the brain from the bloodstream, and it is designed to protect the brain from harmful substances that could cause harm. However, glucose is an essential fuel for the brain, and it is necessary for maintaining the brain's energy supply.

SLC22A6 is expressed in the brain and is involved in the delivery of glucose to the brain's cells. It is also involved in the removal of glucose that has been used by the brain and is stored in the liver. SLC22A6 is regulated by several different factors, including blood glucose levels, insulin signaling, and cellular signaling pathways.

Dysfunction of SLC22A6

SLC22A6 dysfunction has been implicated in the development and progression of several neurological conditions, including diabetes, Alzheimer's disease, and Parkinson's disease. These conditions are characterized by the progressive loss of brain cells, which can lead to a range of symptoms, including cognitive decline, behavior changes, and loss of function.

SLC22A6 dysfunction can occur at multiple levels, including gene level, cellular level and whole animal level. For example, studies have shown that SLC22A6 levels are decreased in the brains of individuals with Alzheimer's disease, and that this decrease is associated with the progression of the disease. Similarly, SLC22A6 dysfunction has been implicated in the development of Parkinson's disease, which is characterized by the progressive loss of brain cells that control movement and other motor functions.

SLC22A6 is also involved in the regulation of cellular signaling pathways, which are responsible for transmitting signals from the brain to the rest of the body. Studies have shown that SLC22A6 is involved in the regulation of several key signaling pathways, including the insulin-IGF- 1 signaling pathway, which is responsible for regulating blood sugar levels.

SLC22A6 as a drug target

SLC22A6 is a

Protein Name: Solute Carrier Family 22 Member 6

Functions: Involved in the renal elimination of endogenous and exogenous organic anions. Functions as organic anion exchanger when the uptake of one molecule of organic anion is coupled with an efflux of one molecule of endogenous dicarboxylic acid (glutarate, ketoglutarate, etc). Mediates the transport of prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) and may be involved in their renal excretion (PubMed:11907186). May contribute to the transport of organic compounds in testes across the blood-testis-barrier (Probable). Mediates the sodium-independent uptake of 2,3-dimercapto-1-propanesulfonic acid (DMPS) (By similarity). Also mediates the sodium-independent uptake of p-aminohippurate (PAH), ochratoxin (OTA), acyclovir (ACV), 3'-azido-3-'deoxythymidine (AZT), cimetidine (CMD), 2,4-dichloro-phenoxyacetate (2,4-D), hippurate (HA), indoleacetate (IA), indoxyl sulfate (IS) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF), cidofovir, adefovir, 9-(2-phosphonylmethoxyethyl) guanine (PMEG), 9-(2-phosphonylmethoxyethyl) diaminopurine (PMEDAP) and edaravone sulfate. PAH uptake is inhibited by p-chloromercuribenzenesulphonate (PCMBS), diethyl pyrocarbonate (DEPC), sulindac, diclofenac, carprofen, glutarate and okadaic acid (By similarity). PAH uptake is inhibited by benzothiazolylcysteine (BTC), S-chlorotrifluoroethylcysteine (CTFC), cysteine S-conjugates S-dichlorovinylcysteine (DCVC), furosemide, steviol, phorbol 12-myristate 13-acetate (PMA), calcium ionophore A23187, benzylpenicillin, furosemide, indomethacin, bumetamide, losartan, probenecid, phenol red, urate, and alpha-ketoglutarate

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•   expression level;
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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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