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transient receptor potential cation channel subfamily M member 4

ה TRPM4 gene provides instructions for making a protein called transient receptor potential cation channel subfamily M member 4 (TRPM4). This protein acts as a channel, opening and closing at specific times to control the flow of positively charged atoms (cations) into and out of cells. The TRPM4 channel is embedded in the outer membrane of cells throughout the body, but it is abundant in heart (cardiac) cells and plays key roles in these cells' ability to generate and transmit electrical signals. TRPM4 channels play a major role in signaling the start of each heartbeat, coordinating the contractions of the upper and lower chambers of the heart, and maintaining a normal heart rhythm.

Normal function

ה TRPM4 gene provides instructions for making a protein called transient receptor potential cation channel subfamily M member 4 (TRPM4). This protein acts as a channel, opening and closing at specific times to control the flow of positively charged atoms (cations) into and out of cells. The TRPM4 channel is embedded in the outer membrane of cells throughout the body, but it is abundant in heart (cardiac) cells and plays key roles in these cells' ability to generate and transmit electrical signals. TRPM4 channels play a major role in signaling the start of each heartbeat, coordinating the contractions of the upper and lower chambers of the heart, and maintaining a normal heart rhythm.

In addition to regulating electric signaling in the heart, the TRPM4 channel is important for the normal functioning of the immune system, the nervous system, the kidneys, and the pancreas.

Conditions referring to this gene or chromosome

Other names

calcium-activated non-selective cation channel 1

hTRPM4

long transient receptor potential channel 4

LTrpC4

melastatin-4

transient receptor potential cation channel, subfamily M, member 4

TRPM4_HUMAN

TRPM4B

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היסטוריית המאמר

המידע בעמוד זה נכתב ונבדק על ידי קלינאים מוסמכים.
  • 18 Aug 2020 | הגרסה האחרונה
  • 1 Apr 2015 | פורסם במקור

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