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C247Y
loss of the ability of the plastidial enzyme to restore growth to JC201, suggests that C247 is essential for activity
D199A
the mutant fails to grow beyond 0.04 D600 after transfer to the non-permissive temperature. D199 is essential for the ability of the plastidial enzyme to complement the defective acyltransferase activity of JC201
E266A
the plastidial enzyme containing this mutation is unable to complement the temperature-sensitive phenotype of JC201, indicating an essential role for this acidic residue
G140S
loss of the ability of the plastidial enzyme to restore growth to JC201, suggests that G140 is essential for activity
H194A
the mutant fails to grow beyond 0.04 D600 after transfer to the non-permissive temperature. H194 is essential for the ability of the plastidial enzyme to complement the defective acyltransferase activity of JC201
K84Q
greatly impaired growth rate, possibly indicating an importance of the N-terminus of the mature protein in determining enzyme activity
L203P
loss of the ability of the plastidial enzyme to restore growth to JC201, suggests that L203 is essential for activity
P187L
loss of the ability of the plastidial enzyme to restore growth to JC201, suggests that P187 is essential for activity
R92G
greatly impaired growth rate, possibly indicating an importance of the N-terminus of the mature protein in determining enzyme activity
T122A
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the change increases the substrate specificity in vitro for oleoyl-CoA and linoleoyl-CoA
T122L
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the change increases the substrate specificity in vitro for lignoceroyl-CoA
140delF
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34.8% of wild-type activity
221delGT
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5% of wild-type activity
252delMRT
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3.2% of wild-type activity
A239V
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90% of wild-type activity
D168R
-
site-directed mutagenesis, the mutant shows slightly increased activity compared to the wild-type AGPAT8
D180fsX251
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7.7% of wild-type activity
E260K
-
site-directed mutagenesis, mutation found in Chanarin-Dorfman syndrome patients, mutation without significant effect on acyltransferase activity
G136R
-
40.3% of wild-type activity
I208A
mutant of human AGPAT1
L228P
-
23.7% of wild-type activity
P207L
mutant of human AGPAT1
Q130P
-
site-directed mutagenesis, mutation found in Chanarin-Dorfman syndrome patients, mutation without significant effect on acyltransferase activity
R149K
mutant of human AGPAT1
R68X
-
14.2% of wild-type activity
T180S
mutant of human AGPAT1
V167fsX228
-
14.9% of wild-type activity
additional information
identification of a null allele lpat2 having a T-DNA inserted into LPAT2, the heterozygous mutant LPAT2/lpat2 has a minimal altered vegetative phenotype but produces shorter siliques that contain normal seeds and remnants of aborted ovules in a 1:1 ratio, overview, lpat2 causes lethality in the female gametophyte but not the male gametophyte, which has the redundant LPAT3, that complements, phenotypes, overview
additional information
identification of a null allele lpat2 having a T-DNA inserted into LPAT2, the heterozygous mutant LPAT2/lpat2 has a minimal altered vegetative phenotype but produces shorter siliques that contain normal seeds and remnants of aborted ovules in a 1:1 ratio, overview, lpat2 causes lethality in the female gametophyte but not the male gametophyte, which has the redundant LPAT3, that complements, phenotypes, overview
additional information
identification of a null allele lpat2 having a T-DNA inserted into LPAT2, the heterozygous mutant LPAT2/lpat2 has a minimal altered vegetative phenotype but produces shorter siliques that contain normal seeds and remnants of aborted ovules in a 1:1 ratio, overview, lpat2 causes lethality in the female gametophyte but not the male gametophyte, which has the redundant LPAT3, that complements, phenotypes, overview
additional information
identification of a null allele lpat2 having a T-DNA inserted into LPAT2, the heterozygous mutant LPAT2/lpat2 has a minimal altered vegetative phenotype but produces shorter siliques that contain normal seeds and remnants of aborted ovules in a 1:1 ratio, overview, lpat2 causes lethality in the female gametophyte but not the male gametophyte, which has the redundant LPAT3, that complements, phenotypes, overview
additional information
identification of a null allele lpat2 having a T-DNA inserted into LPAT2, the heterozygous mutant LPAT2/lpat2 has a minimal altered vegetative phenotype but produces shorter siliques that contain normal seeds and remnants of aborted ovules in a 1:1 ratio, overview, lpat2 causes lethality in the female gametophyte but not the male gametophyte, which has the redundant LPAT3, that complements, phenotypes, overview
additional information
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identification of a null allele lpat2 having a T-DNA inserted into LPAT2, the heterozygous mutant LPAT2/lpat2 has a minimal altered vegetative phenotype but produces shorter siliques that contain normal seeds and remnants of aborted ovules in a 1:1 ratio, overview, lpat2 causes lethality in the female gametophyte but not the male gametophyte, which has the redundant LPAT3, that complements, phenotypes, overview
additional information
LPAT3-cDNA functionally complements the lpat2 LPAT2 mutant strain in part in heterozygous LPAT2/lpat2 and homozygous lpat2/lpat2 mutants, overview
additional information
LPAT3-cDNA functionally complements the lpat2 LPAT2 mutant strain in part in heterozygous LPAT2/lpat2 and homozygous lpat2/lpat2 mutants, overview
additional information
LPAT3-cDNA functionally complements the lpat2 LPAT2 mutant strain in part in heterozygous LPAT2/lpat2 and homozygous lpat2/lpat2 mutants, overview
additional information
LPAT3-cDNA functionally complements the lpat2 LPAT2 mutant strain in part in heterozygous LPAT2/lpat2 and homozygous lpat2/lpat2 mutants, overview
additional information
LPAT3-cDNA functionally complements the lpat2 LPAT2 mutant strain in part in heterozygous LPAT2/lpat2 and homozygous lpat2/lpat2 mutants, overview
additional information
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LPAT3-cDNA functionally complements the lpat2 LPAT2 mutant strain in part in heterozygous LPAT2/lpat2 and homozygous lpat2/lpat2 mutants, overview
additional information
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adenine-440 is responsible for the temperature sensitive lesion in the enzyme activity of JC201. Conversion of the mutant adenine-440 back to the native guanine-440 nucleotide restores the enzyme activity at the non-permissive temperature of 42°C
additional information
small interference RNA-mediated knockdown of AGPAT2 expression in OP-9 cells prevents appropriate early induction of C/EBPbeta and PPARgamma, key transcriptional activators of the adipogenic program, and delays expression of multiple adipocyte-related genes
additional information
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generation of stable Huh-7 cells with a knockout for AGPAT2 activity by shRNA-AGPAT2-lentivirus
additional information
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overexpression of LPAAT3 in HeLa cells significantly inhibits the formation of Golgi membrane tubules in vivo and in vitro. Anterograde and retrograde protein trafficking is slower in cells overexpressing LPAAT3 and accelerated in cells with expression reduced by siRNA, LPAAT3 knockdown leads to Golgi fragmentation, overview
additional information
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recombinant expression of murine CGI-58 in fibroblasts from humans with Chanarin-Dorfman syndrome increases the incorporation of radiolabeled fatty acids released from the lipolysis of stored triacylglycerols into phospholipids
additional information
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enhanced sn-2 distribution of docosahexaenoic acid in transgenic Arabidopsis thaliana seed triacylgycerols by expression of Mortierella alpina MaLPAAT
additional information
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recombinant expression of murine CGI-58 in fibroblasts from humans with Chanarin-Dorfman syndrome increases the incorporation of radiolabeled fatty acids released from the lipolysis of stored triacylglycerols into phospholipids
additional information
recombinant expression of murine CGI-58 in fibroblasts from humans with Chanarin-Dorfman syndrome increases the incorporation of radiolabeled fatty acids released from the lipolysis of stored triacylglycerols into phospholipids
additional information
KX256278
recombinant overexpression of gene PrLPAAT1 in Arabidopsis thaliana transgenic plant seeds increases total fatty acid (FA) content and the main fatty acid accumulation. Most of the FAs have higher levels of production in the transgenic T1 seeds compared to wild-type seeds, and the predominant FAs in the transgenic seeds are C18:1, C18:2, C18:3, C20:1, and C16:0
additional information
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recombinant overexpression of gene PrLPAAT1 in Arabidopsis thaliana transgenic plant seeds increases total fatty acid (FA) content and the main fatty acid accumulation. Most of the FAs have higher levels of production in the transgenic T1 seeds compared to wild-type seeds, and the predominant FAs in the transgenic seeds are C18:1, C18:2, C18:3, C20:1, and C16:0
additional information
generation of a plsC4-disrupted mutant, phenotype, overview
additional information
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generation of a plsC4-disrupted mutant, phenotype, overview
additional information
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generation of a plsC4-disrupted mutant, phenotype, overview
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additional information
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construction of a PlsC knockout mutant, which shows 25fold decreased phosphatidylglycerols 18:1/16:0 ratio, phospholipid composition of mutant relative to wild-type cells, overview