EC Number   |
Protein Variants |
Reference |
|---|
   3.4.23.B24 | D265A |
inactive. Signal peptides are trapped by the catalytically inactive SPP mutant. Preproteins and misfolded membrane proteins interact with both wild-type SPP and the mutant |
717212 |
| 3.4.23.B24 | D337A |
site-directed mutagenesis, inactive mutant |
-, 754762 |
| 3.4.23.B24 | K199A |
active site mutant |
-, 733343 |
| 3.4.23.B24 | K199A |
inactive |
-, 734471 |
| 3.4.23.B24 | more |
construction of C-terminal deletion mutants DELTA329-335, DELTA307-335 and DELTA295-335. The C-terminus is not essential for oligomerization of the enzyme |
-, 733343 |
| 3.4.23.B24 | more |
endogenous SPP expression is not affected by human SPPL2c overexpression |
753429 |
| 3.4.23.B24 | more |
generation of a knockout enzyme null mutant DELTAsppA |
-, 754762 |
| 3.4.23.B24 | more |
generation of constitutive SPP knockout mice. The constitutive knockout of this protease leads to embryonic lethality after day 13.5, however without apparent histological abnormalities in the SPP-/- mouse embryos. At least in immortalised, continuously proliferating cell lines a loss of SPP and any potentially resulting proteostatic dysbalance can be compensated |
752819 |
| 3.4.23.B24 | more |
generation of constitutive SPPL2a knockout mice. Constitutive SPPL2a knockout mice are viable. Three different strains of SPPL2a-deficient mice are generated by gene targeting or derived from N-ethyl-N-nitrosourea (ENU) mutagenesis screens. All three models exhibit a characteristic B cell differentiation defect that manifests during the so-called transitional (T) stages of splenic B cell maturation which these cells have to pass through prior to becoming mature, antigen-reactive B cells. Whereas the T1 population is largely preserved in SPPL2a-/- mice, T2 B cells as well as subsequent stages like the mature B cells are significantly depleted. In addition to this maturation block of the follicular B cells also innate-like B cell populations like the marginal zone and B1 B cells are significantly reduced in SPPL2a-deficient mice so that these mice are characterised by a global depletion of B lymphocytes. Also the remaining B cells exhibit a major functional deficit, antibody production and humoral immune responses are significantly impaired. Double knockout of SPPL2a and SPPL2b. SPPL2a/b double-deficient mice are viable, without any overt disability and exhibit the phenotypic changes associated with the loss of SPPL2a |
752819 |
| 3.4.23.B24 | more |
generation of constitutive SPPL2b knockout mice that show no obvious phenotype. Double knockout of SPPL2a and SPPL2b. SPPL2a/b double-deficient mice are viable, without any overt disability and exhibit the phenotypic changes associated with the loss of SPPL2a |
752819 |
