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Literature summary for 2.7.1.56 extracted from
- Human H+ATPase a4 subunit mutations causing renal tubular acidosis reveal a role for interaction with phosphofructokinase-1 (2008), Am. J. Physiol. Renal Physiol., 295, F950-F958.
Natural Substrates/ Products (Substrates)
| Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| additional information | Homo sapiens | important role for PFK-1 in normal proton pump function. Loss of a-subunit/PFK-1 interaction is likely to decrease the stability of the metabolon formed by various H+ATPase subunits (notably E and a) and glycolytic components (aldolase and PFK-1) | ? | - |
? |  |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | - |
- |
- |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| additional information | important role for PFK-1 in normal proton pump function. Loss of a-subunit/PFK-1 interaction is likely to decrease the stability of the metabolon formed by various H+ATPase subunits (notably E and a) and glycolytic components (aldolase and PFK-1) | Homo sapiens | ? | - |
? | |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| PFK-1 | - |
Homo sapiens |
| phosphofructokinase-1 | - |
Homo sapiens |
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