3.4.23.B24: signal peptide peptidase
This is an abbreviated version!
For detailed information about signal peptide peptidase, go to the full flat file.
Word Map on EC 3.4.23.B24
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3.4.23.B24
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aspartyl
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presenilins
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intramembrane-cleaving
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gamma-secretase
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sppl2a
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medicine
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gxgd-type
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spp-mediated
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bri2
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i-clips
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presenilin-like
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site-2
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pharmacology
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analysis
- 3.4.23.B24
-
aspartyl
-
presenilins
-
intramembrane-cleaving
- gamma-secretase
- sppl2a
- medicine
-
gxgd-type
-
spp-mediated
- bri2
- i-clips
-
presenilin-like
-
site-2
- pharmacology
- analysis
Reaction
intramembrane cleavage of signal peptides =
Synonyms
ANID_08681, aspartic intramembrane protease, Hm13, hSPP, minor histocompatibility antigen H13, PF3D7_1457000, PlSPP, signal peptide peptidase like 2a, signal peptide peptidase-like 2a, signal peptide peptidase-like 2B, signal peptide peptidase-like 2C, signal peptide peptidase-like 3, SPP, SPP-like 2A, SPP-like 2B, SPP-like 2C, SPP-like 3, SPP1, SppA, SPPL, SPPL2a, SPPL2b, SPPL2c, UMAG_02729
ECTree
3.4.23.B24 signal peptide peptidaseAdvanced search results
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results (Engineering
Engineering on EC 3.4.23.B24 - signal peptide peptidase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
D337A
K199A
K199A
D265A
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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
additional information
additional information
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generation of a knockout enzyme null mutant DELTAsppA
additional information
Aspergillus nidulans A773
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generation of a knockout enzyme null mutant DELTAsppA
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additional information
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improvement of protein secretion via overexpression of the SppA signal peptide peptidase in Bacillus licheniformis. Enzyme knockout of gene sppA, encoding the signal peptide peptidase, individually in Bacillus licheniformis strain BL10. Overexpression of sppA could not only improve the protein secretion level, but also enhance the biomass yield
additional information
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improvement of protein secretion via overexpression of the SppA signal peptide peptidase in Bacillus licheniformis. Enzyme knockout of gene sppA, encoding the signal peptide peptidase, individually in Bacillus licheniformis strain BL10. Overexpression of sppA could not only improve the protein secretion level, but also enhance the biomass yield
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additional information
construction of C-terminal deletion mutants DELTA329-335, DELTA307-335 and DELTA295-335. The C-terminus is not essential for oligomerization of the enzyme
additional information
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construction of C-terminal deletion mutants DELTA329-335, DELTA307-335 and DELTA295-335. The C-terminus is not essential for oligomerization of the enzyme
additional information
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construction of C-terminal deletion mutants DELTA329-335, DELTA307-335 and DELTA295-335. The C-terminus is not essential for oligomerization of the enzyme
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additional information
endogenous SPP expression is not affected by human SPPL2c overexpression
additional information
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lung (H-1299) and breast (MCF-7 and MDA-MB-231) cancer cell lines with stable SPP knockdown mediated by two different specific shRNAs targeting SPP are established. Stable depletion of SPP expression in lung and breast cancer cell lines significantly reduces cell growth and migration/invasion abilities
additional information
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
additional information
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
additional information
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
additional information
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
additional information
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
additional information
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
additional information
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
additional information
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
additional information
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
additional information
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
additional information
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
additional information
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
additional information
generation of constitutive SPPL3 knockout mice from different strains
additional information
generation of constitutive SPPL3 knockout mice from different strains
additional information
generation of constitutive SPPL3 knockout mice from different strains
additional information
generation of constitutive SPPL3 knockout mice from different strains
additional information
proteolytic processing by SPPL2c impairs vesicular transport and causes retention of cargo proteins in the endoplasmic reticulum in recombinant SPPL2c-overexpessing HEK-293 cells. As a consequence, the integrity of subcellular compartments, in particular the Golgi, is disturbed. Quantification of pre-acrosomal structures in seminiferous tubular cross sections in wild-type and SPPL2c-lacking cells
additional information
proteolytic processing by SPPL2c impairs vesicular transport and causes retention of cargo proteins in the endoplasmic reticulum in recombinant SPPL2c-overexpessing HEK-293 cells. As a consequence, the integrity of subcellular compartments, in particular the Golgi, is disturbed. Quantification of pre-acrosomal structures in seminiferous tubular cross sections in wild-type and SPPL2c-lacking cells
additional information
generation of DELTAspp1 strains. DELTAspp1 strains do not show increased expression of fungal UPR marker genes in planta. DELTAspp1 strains are not impaired in H2O2 resistance
additional information
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generation of DELTAspp1 strains. DELTAspp1 strains do not show increased expression of fungal UPR marker genes in planta. DELTAspp1 strains are not impaired in H2O2 resistance
additional information
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generation of DELTAspp1 strains. DELTAspp1 strains do not show increased expression of fungal UPR marker genes in planta. DELTAspp1 strains are not impaired in H2O2 resistance
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additional information
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generation of DELTAspp1 strains. DELTAspp1 strains do not show increased expression of fungal UPR marker genes in planta. DELTAspp1 strains are not impaired in H2O2 resistance
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