7.6.2.1: P-type phospholipid transporter
This is an abbreviated version!
For detailed information about P-type phospholipid transporter, go to the full flat file.
Word Map on EC 7.6.2.1
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7.6.2.1
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leaflet
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cholestasis
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aminophospholipids
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bile
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asymmetry
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erythrocyte
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intrahepatic
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atpases
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ca2+-atpase
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na+
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myosin
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biliary
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canalicular
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abcb11
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k+-atpase
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phosphatidylethanolamine
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scramble
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actin-activated
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actomyosin
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ca2+-dependent
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flip-flop
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p-glycoproteins
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na+,k+-atpase
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pro12ala
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ca2+-activated
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ursodeoxycholic
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cholelithiasis
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ouabain
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hepatobiliary
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exoplasmic
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gallstone
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o-antigens
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pruritus
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gizzard
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proteoliposomes
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lipid-linked
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cholangiopathy
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meromyosin
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3.6.1.3
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actin-myosin
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ptdser
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ppargamma2
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ca2+-stimulated
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superprecipitation
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fr
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ca2+-pumping
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analysis
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prothrombinase
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photophosphorylation
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molecular biology
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undecaprenyl
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medicine
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subfragment-1
- 7.6.2.1
- leaflet
- cholestasis
-
aminophospholipids
- bile
-
asymmetry
- erythrocyte
-
intrahepatic
- atpases
- ca2+-atpase
- na+
- myosin
- biliary
-
canalicular
-
abcb11
-
k+-atpase
- phosphatidylethanolamine
-
scramble
-
actin-activated
- actomyosin
-
ca2+-dependent
-
flip-flop
- p-glycoproteins
- na+,k+-atpase
-
pro12ala
-
ca2+-activated
-
ursodeoxycholic
- cholelithiasis
- ouabain
- hepatobiliary
-
exoplasmic
- gallstone
-
o-antigens
- pruritus
- gizzard
-
proteoliposomes
-
lipid-linked
-
cholangiopathy
- meromyosin
-
3.6.1.3
-
actin-myosin
-
ptdser
-
ppargamma2
-
ca2+-stimulated
-
superprecipitation
- fr
-
ca2+-pumping
- analysis
- prothrombinase
-
photophosphorylation
- molecular biology
- undecaprenyl
- medicine
-
subfragment-1
Reaction
Synonyms
ABCB1, ABCB4, ALA1, ALA10, ALA11, ALA12, ALA2, ALA3, ALA4, ALA5, ALA7, ALA8, ALA9, aminophospholipid ATPase, aminophospholipid flippase, aminophospholipid flippase 10, aminophospholipid flippase 11, aminophospholipid flippase 12, aminophospholipid scramblase, aminophospholipid translocase, aminophospholipid translocase VC, aminophospholipid transporter, aminophospholipid-translocase, aminophosphoplipid translocase, APLT, ATP phosphohydrolase (phospholipid-flipping), ATP-dependent specific phospholipid flippase, ATP-independent flippase, ATP-independent long-chain phosphatidylcholine translocator, ATP10A, ATP10B, ATP10D, ATP11A, ATP11B, ATP11C, ATP8A1, Atp8a2, ATP8B1, ATP8B2, ATP8B3, ATP8B4, ATP8B5, ATP9A, ATP9B, ATPase II, ATPVC, ATPVD, CDC50A, Cdc50p-Drs2p, Cfs1p, Dnf1, Dnf1 |, Dnf1p, Dnf1p and Dnf2p, Dnf1p-Lem3p, Dnf2, Dnf2p, Dnf3, Dnf3p, Drs2, Drs2-dependent phosphatidylserine translocase, Drs2p, EC 3.6.3.1, EC 3.6.3.13, energy-dependent lipid flippase, energy-independent lipid flippase, EpsE, erythroid ATP-dependent aminophospholipid transporter, flippase, glycerophospholipid flippase, HUSSY-20, inward-directed phospholipid translocase, LdMT, LdRos3, lipid flippase, LMT translocase, M5-DLO flippase, Man5GlcNAc2-PP-dolichol flippase, MDR3 P-glycoprotein, Mg2+-ATPase, Mg2+-ATPase A, miltefosine transporter, More, MsbA, multidrug resistance 3 P-glycoprotein, MurJ, MviN, Neo1, Neo1p, P type aminophospholipid transporter, P-glycoprotein, P-gp, P4 ATPase ALA1, P4-ATPase, P4-type ATPase, PC-flippase, peptidoglycan lipid II flippase, phosphatidylserine flippase, phosphatidylserine translocase, phosphatidylserine translocase/ATPase, phospholipid flippase, phospholipid scramblase, phospholipid scramblase 1, phospholipid scramblase 3, phospholipid scrambling activity, phospholipid translocase, phospholipid-translocase, phospholipid-translocating ATPase, phospholipid-transporting ATPase IB, PL flippase, PL scramblase, PLS3, PLSCR1, PLSCR2, PLSCR3, PLSCR4, PS flippase, PS translocase, PS-flippase, scramblase, SCRM-1, sphingomyelin flippase, TAT-1, TAT-2, TAT-3, TAT-4, TAT-5, TAT-6, transbilayer amphipath transporter, transbilayer amphipath transporter-1, type 4 P-type ATPas, type II secretion ATPase, type IV P-type ATPase
ECTree
7.6.2.1 P-type phospholipid transporterAdvanced search results
results (
results (Engineering
Engineering on EC 7.6.2.1 - P-type phospholipid transporter
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
E126A
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the mutant shows about 10% of wild type activity. The mutation leads to reduced glycosylation of the accessory subunit CDC50A
I115A
biphasic phosphatidylserine concentration dependence with inhibition at the highest concentration
I305A
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the mutant shows about 50% of wild type activity. The mutation leads to reduced glycosylation of the accessory subunit CDC50A
I362A
I364Q
activation phase is followed by an inhibition phase at high phosphatidylserine concentration
L112A
mutation does not appreciably affect Vmax, the apparent affinities for the substrates, or the phosphorylation rate
L361A
L366A
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the mutant shows about 40% of wild type activity. The mutation leads to reduced glycosylation of the accessory subunit CDC50A
L367A
S1138D
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the mutant shows slightly reduced activity compared to the wild type enzyme
V906A
pronounced inhibition at high phosphatidylethanol concentration with only a slight inhibition at high phosphatidylserine concentration
Y878A
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the mutant shows about 25% of wild type activity. The mutation leads to reduced glycosylation of the accessory subunit CDC50A
A270T
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mutant and wild-type enzymes have similar activities at 30°C, but the mutant activity is decreased significant at 42°C
F258V
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site-directed mutagenesis, mutation of the calcium binding motif abolishes the lipid flip-flop activity of PLS3, a dominant negative mutant of PLS3, expression of the PLS3(F258V) mutant in HEK-293 cells results in a phenotype still consistent with low PLS3 activity despite the presence of normal PLS3 in these cells due to spontaneous rate of flip-flop
I376M
missense mutation identified in a patient with cerebellar ataxia, mental retardation and dysequilibrium syndrome. The mutation lies in a highly conserved C-terminal transmembrane region of E1 E2 ATPase domain
K1075M
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site-directed mutagenesis in the Walker A motif results in an inactive mutant
K435M
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site-directed mutagenesis in the Walker A motif results in an inactive mutant
E181Q
the mutant shows strongly reduced activity compared to the wild type enzyme
E186Q
inactive
G308V
Atp8b1 protein is virtually undetectable in G308V mouse liver, the G308V substitution results in an instable protein that cannot exit the endoplasmic reticulum and is broken down by the proteasome
D256E
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the mutant shows reduced activity with phosphatidylcholine, increased activity with phosphatidylserine, and increased activity with sphingomyelin compared to the wild type enzyme
F213S
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the mutant shows increased activity with phosphatidylcholine, phosphatidylserine, and sphingomyelin compared to the wild type enzyme
F511L
the mutant has a specific activity that is 35% that of wild type Drs2
F511Y
the mutant retains wild type activity, the substitution in Drs2 specifically abrogates phosphatidylserine recognition by this flippase causing phosphatidylserine exposure on the outer leaflet of the plasma membrane without disrupting phospatidylethanolamine asymmetry
I1235F
mutation increases the overall activity of Dnf1 for all substrates and causes partial loss of specificity for glycerophospholipid
I615S
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the mutation significantly increases sphingomyelin and phosphatidylserine transport compared to the wild type enzyme
L242S
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the mutant shows reduced activity with phosphatidylcholine and wild type activity with sphingomyelin
N220C
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the mutant shows wild type activity with phosphatidylcholine and increased activity with sphingomyelin
N220S
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the mutant shows reduced activity with phosphatidylcholine and increased activity with sphingomyelin compared to the wild type enzyme
N220S/L242S
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the mutant shows reduced activity with phosphatidylcholine and increased activity with sphingomyelin compared to the wild type enzyme
N220T
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the mutant shows increased activity with phosphatidylcholine and increased activity with sphingomyelin compared to the wild type enzyme
N550S
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the mutant shows reduced activity with phosphatidylcholine, increased activity with phosphatidylserine, and increased activity with sphingomyelin compared to the wild type enzyme
T254A
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the mutant shows reduced activity with phosphatidylcholine, increased activity with phosphatidylserine, and increased activity with sphingomyelin compared to the wild type enzyme
Y618F
acquisition of the phosphatidylserine substrate maps to a Tyr618Phe substitution in transmembrane segment 4 of Dnf1. The rate of 7-nitrobenz-2oxa-1,3-diazol-4-yl phospholipid uptake by Dnf1 Y618F is comparable to wild type Dnf1
additional information
L361A
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the mutant shows about 15% of wild type activity. The mutation leads to reduced glycosylation of the accessory subunit CDC50A
additional information
phenotypic and genetic analyses of multiple itb2 alleles, including the T-DNA insertion alleles, shows that the loss of ITB2/ALA3 function leads to aberrant trichome expansion, reduced primary root growth and longer root hairs, but has no effect on plant growth, phenotype, overview
additional information
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construction of two deletion null mutants of scrm-1, mutants tm698 and tm805, which show more cell corpse than the wild-type embryos and a defect in cell corps engulfment, the average cell corpse duration in mutant scrm-1 tm698 is 55 min, in mutant scrm-1 tm805 57 in, and in wild-type embryos 33 min. The mutants also show highly decreased externalization of phosphatidylserine on the surface of apoptotic germ cells, phenotypes, overview
additional information
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knock-out of the tat-1 gene results in abolishes phosphatidylserine exposure on apoptotic cells and reduced efficiency of cell-corps clearance during embryonic development and in the hermaphrodite germ line, overview
additional information
a disruption of PLSCR3 gene diminishes the translocation of CL from inner membrane to the outer membrane in cultured HeLa cells, and also decreases their sensitivity to UV and t-Bid induced apoptosis
additional information
a disruption of PLSCR3 gene diminishes the translocation of CL from inner membrane to the outer membrane in cultured HeLa cells, and also decreases their sensitivity to UV and t-Bid induced apoptosis
additional information
a disruption of PLSCR3 gene diminishes the translocation of CL from inner membrane to the outer membrane in cultured HeLa cells, and also decreases their sensitivity to UV and t-Bid induced apoptosis
additional information
a disruption of PLSCR3 gene diminishes the translocation of CL from inner membrane to the outer membrane in cultured HeLa cells, and also decreases their sensitivity to UV and t-Bid induced apoptosis
additional information
mutations in isozyme ATP8B1 cause progressive familial intrahepatic cholestasis type 1 and benign recurrent intrahepatic cholestasis type 1, overview
additional information
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construction of a chimeric ATP9 protein by replacement of the N-terminal cytoplasmic region of ATP9A with the corresponding region of ATP9B, the mutant chimera is localized exclusively to the Golgi apparatus. The mutant ATP9B(53-126) construct retains the ability to localize to the Golgi
additional information
a gene disruption mutation leads to mental retardation and severe hypotonia
additional information
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a gene disruption mutation leads to mental retardation and severe hypotonia
additional information
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lem3 mutants are not affected in Lem3p-Dnf1p complex formation, but show a synthetic growth defect with the null mutation CDC50, overview
additional information
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simultaneous inactivation of Dnf2p and Dnf1p abolishes the ATP-dependent influx of phosphatidylserine and phosphatidylethanolamine into the cell
additional information
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a conditional allele that inactivates Drs2p phospholipid translocase activity disrupts its own transport in this AP-1 pathway, missorting of Drs2p to the plasma membrane of AP-1 mutants, cell surface accumulation of GFP-Drs2p is less pronounced in apm1DELTA and nearly absent in apm2DELTA cells treated with latrunculin A, overview
additional information
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construction of deletion mutants of phosphilipid translocases and CDC50 proteins, phenotypes, detailed overview
additional information
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construction of yeast knockout strains lacking Drs2p and/or Drf1p activity, the pan1-20 temperature-sensitive mutant is constitutively defective for Ub-dependent endocytosis but is not defective for NPFXD-dependent endocytosis at the permissive growth temperature. To sustain viability of pan1-20, Drs2p must be endocytosed through the NPFXD/Sla1p pathway
additional information
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deletion mutants of drs2 and cdc50, DELTAdrs2 and DELTAcdc50, exhibit a clathrin-deficient phenotype with delayed transport of carboxypeptidase Y to the vacuole, mislocation of resident TGN enzymes and the accumulation of aberrant membrane structures, the mutations cause a loss in plasma membrane phosphatidylserine asymmetry leading to disruption of protein trafficking, phenotypes, overview
additional information
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loss of P4 ATPases Drs2p and Dnf3p disrupts aminophospholipid transport and asymmetry in yeast post-Golgi secretory vesicles, removal of P4 ATPases Dnf1p and Dnf2p from budding yeast abolishes inward translocation of 6-[(7-nitrobenz-2-oxa-1,3-diazol-4-yl)aminocaproyl] (NBD)-labeled phosphatidylserine, phosphatidylethanolamine, and phosphatidylcholine across the plasma membrane and causes cell surface exposure of endogenous phosphatidylethanolamine, overview
additional information
generation of chimeras between isoforms Drs2 and Dnf1 by swapping of transmembrane domains. The mechanistic coupling of the entry and the exit gates seems to be conserved for Drs2. The residues that determine headgroup specificity for phospholipid transport cluster at two interfacial regions flanking transmembrane segments 1-4 and lie outside of the canonical substrate binding site operating in cation pumps. Two substrate-selecting gates act sequentially on opposite sides of the membrane: an entry gate, where phospholipid is initially selected from the extracellular leaflet, and an exit gate at the cytosolic leaflet. The entry and exit gates act cooperatively but imperfectly For example, the entry gate QQ to GA mutation causes a specific loss of phosphatidylserine asymmetry that can be restored by the N445S exit gate mutation
additional information
generation of chimeras between isoforms Drs2 and Dnf1 by swapping of transmembrane domains. The mechanistic coupling of the entry and the exit gates seems to be conserved for Drs2. The residues that determine headgroup specificity for phospholipid transport cluster at two interfacial regions flanking transmembrane segments 1-4 and lie outside of the canonical substrate binding site operating in cation pumps. Two substrate-selecting gates act sequentially on opposite sides of the membrane: an entry gate, where phospholipid is initially selected from the extracellular leaflet, and an exit gate at the cytosolic leaflet. The entry and exit gates act cooperatively but imperfectly For example, the entry gate QQ to GA mutation causes a specific loss of phosphatidylserine asymmetry that can be restored by the N445S exit gate mutation
additional information
generation of chimeras between isoforms Drs2 and Dnf1 by swapping of transmembrane domains. Within the entry gate, residues specifically involved in the phosphatidylcholine preference of Dnf1 are Ile234, Phe235, Pro240, Gly241, Tyr575, Glu586, Phe587, Gly588, and Ile590, and involved in suppression of phosphatidylserine recognition are Gly230, Ala231, and K578. Within the exit gate, residues responsible for phosphatidylcholine preference are Ile545 and Glu622 and for suppression of phosphatidylserine transport are Tyr618, Asn550, Val621, and Glu622
additional information
generation of chimeras between isoforms Drs2 and Dnf1 by swapping of transmembrane domains. Within the entry gate, residues specifically involved in the phosphatidylcholine preference of Dnf1 are Ile234, Phe235, Pro240, Gly241, Tyr575, Glu586, Phe587, Gly588, and Ile590, and involved in suppression of phosphatidylserine recognition are Gly230, Ala231, and K578. Within the exit gate, residues responsible for phosphatidylcholine preference are Ile545 and Glu622 and for suppression of phosphatidylserine transport are Tyr618, Asn550, Val621, and Glu622
additional information
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deletion mutants of drs2 and cdc50, DELTAdrs2 and DELTAcdc50, exhibit a clathrin-deficient phenotype with delayed transport of carboxypeptidase Y to the vacuole, mislocation of resident TGN enzymes and the accumulation of aberrant membrane structures, the mutations cause a loss in plasma membrane phosphatidylserine asymmetry leading to disruption of protein trafficking, phenotypes, overview
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additional information
-
loss of P4 ATPases Drs2p and Dnf3p disrupts aminophospholipid transport and asymmetry in yeast post-Golgi secretory vesicles, removal of P4 ATPases Dnf1p and Dnf2p from budding yeast abolishes inward translocation of 6-[(7-nitrobenz-2-oxa-1,3-diazol-4-yl)aminocaproyl] (NBD)-labeled phosphatidylserine, phosphatidylethanolamine, and phosphatidylcholine across the plasma membrane and causes cell surface exposure of endogenous phosphatidylethanolamine, overview
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