EC Number   |
General Information |
Reference |
|---|
   5.2.1.8 | evolution |
ROF2 encodes a peptidyl-prolyl cis-trans isomerase of the FK506-binding protein class |
728483 |
| 5.2.1.8 | evolution |
the enzyme belongs to the FK506-binding protein (FKBP) family of peptidyl-prolyl isomerases, PPIases, which share a canonical domain fold consisting of a beta-sheet composed of four large and two small -strands, opposed by a single main alpha-helix |
727957 |
| 5.2.1.8 | evolution |
the enzyme belongs to the FK506-binding protein (FKBP) family whose members are peptidyl-prolyl cis-trans isomerases with the enzymatic function attributed to the FKBP domain. Six members of this family localize to the mammalian endoplasmic reticulum. Four of them, FKBP22 (encoded by the FKBP14 gene), FKBP23 (FKBP7), FKBP60 (FKBP9), and FKBP65 (FKBP10), are unique among all FKBPs as they contain the EF-hand motifs. All FKBP-EFs contain an endoplasmic reticulum retention signal at the C-terminus |
728767 |
| 5.2.1.8 | evolution |
the enzyme belongs to the parvulin family of peptidyl-prolyl cis/trans isomerases, PPIases |
-, 728503 |
| 5.2.1.8 | malfunction |
a DELTAef0685/DELTAef1534 mutant is more resistant to oxidative stress, is able to grow under a high manganese concentration, and shows altered resistance to ampicillin and quinolone antibiotics |
727618 |
| 5.2.1.8 | malfunction |
Bacillus subtilis cells depleted of the PrsA protein are able to grow in the presence of a high concentration of magnesium (20 mM). PrsA depletion destabilizes penicillin-binding proteins |
-, 716254 |
| 5.2.1.8 | malfunction |
knockdown of FKBP1B induces eye formation malfunction |
714800 |
| 5.2.1.8 | malfunction |
knockdown of Pin1 does not prevent CK2alpha phosphorylation |
715712 |
| 5.2.1.8 | malfunction |
loss of function of ROF2, and especially double mutation of ROF2 and the closely related gene ROF1, results in acid sensitivity, stress and development phenotypes of ROF mutants, overview |
728483 |
| 5.2.1.8 | malfunction |
Pin1 blockade leads to Bax cleavage, mitochondrial translocation and caspase 9 and 3 activation, irrespective of the presence of cytokines, and Pin1 blockade accelerates eosinophil apoptosis |
705854 |
