Magnesium transporter protein

"Magnesium transporter protein" is a **generic term** that refers to several families of evolutionarily conserved membrane proteins responsible for the regulated movement of **magnesium ions (Mg2+)** across cellular membranes[2][3][6]. There are multiple well-defined families of magnesium transporters, including the **CorA, MgtA/B (P-type ATPases), MgtE, CorB/C (CNNM in vertebrates), SLC41**, and **TRPM6/7** channels[2][3][6]. These proteins are structurally and mechanistically diverse: some function like channels (CorA, TRPM6/7), some as ATP-driven pumps (MgtA/B), and others (CorB/C, CNNM) act as regulators and possibly as direct transporters[1][2][5]. Their biological roles are critical, as magnesium is an essential intracellular ion needed for many enzymatic reactions, nucleic acid stabilization, and cellular energy production[2][3][5]. Disturbances in Mg2+ transporter activity underlie various human disorders, including hereditary hypomagnesemia, cardiovascular and neurological disease, and impair virulence in pathogenic bacteria[5][2]. Several genetic mutations in human CNNM2 and CNNM4, and altered TRPM6/7 function, are directly associated with clinical disease[5]. The term as given is overly broad; scientific and clinical literature typically specifies the exact protein or gene (e.g., "CorA magnesium transporter", "CNNM2", "TRPM6"). **Note on correctness:** The target "Magnesium transporter protein" is **nonspecific and overly generic**, encompassing a variety of structurally and functionally distinct transporter families[2][3][6]. For detailed or structured data, precise identification of the specific gene/protein (e.g., CNNM2, TRPM6) is required. Where context allows, replace "Magnesium transporter protein" with the full, canonical name of the relevant family member for accuracy and specificity.

Other names

CNNM proteinCorAMgtAMgtBMgtECorBCorCSLC41TRPM6TRPM7

Facilitate or regulate Mg2+ influx or efflux across cellular membranes, in some cases using ATP hydrolysis (P-type ATPases), electrochemical gradients (channels), or through regulated conformational changes. Some TRPM6/7 channels couple transport with kinase activity.