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1 transported to cytosol and incorporated into argininosuccinate.
2 ed with l-citrulline increased the levels of argininosuccinate, an enzyme that metabolizes l-citrulli
3 tained unchanged during the evolution of the argininosuccinate gene are able to change in the pseudog
10 urea cycle disorder caused by deficiency of argininosuccinate lyase (ASL) with a wide clinical spect
11 zed by argininosuccinate synthase (Ass1) and argininosuccinate lyase (Asl), which would lead to abund
12 We show that a hypomorphic mouse model of argininosuccinate lyase (encoded by Asl) deficiency has
13 uals with argininosuccinate synthetase 1 and argininosuccinate lyase deficiencies identified by newbo
14 inate synthetase deficiency (0.22 +/- 0.03), argininosuccinate lyase deficiency (0.35 +/- 0.11), and
15 dge, this is the first report of an acquired argininosuccinate lyase deficiency by liver transplantat
16 inosuccinate synthetase mRNA but did express argininosuccinate lyase mRNA, suggesting that the argini
17 tures in the fumarase superfamily, including argininosuccinate lyase, delta-crystallin, fumarase, and
18 Together, these three enzymes, eNOS, AS, and argininosuccinate lyase, make up the citrulline-NO cycle
19 re identified as argininosuccinate synthase, argininosuccinate lyase, neuronal nitric-oxide synthase,
20 accharomyces cerevisiae counterparts, namely argininosuccinate lyase, PR-aminoimidazolesuccinocarboxa
21 enzymes, argininosuccinate synthase (AS) and argininosuccinate lyase, providing the substrate arginin
22 suppressed pyrimidine biosynthetic pathway, argininosuccinate lyase-encoding, and ABC transporter-re
26 cing, we show that an inflammatory aspartate-argininosuccinate shunt is induced following lipopolysac
27 ne is recycled to l-arginine by two enzymes, argininosuccinate synthase (AS) and argininosuccinate ly
31 used to selectively reduce the expression of argininosuccinate synthase (AS), because the only known
32 pression of the arginine resynthesis enzymes argininosuccinate synthase (ASS) and ornithine transcarb
34 ught to fuel arginine synthesis catalyzed by argininosuccinate synthase (Ass1) and argininosuccinate
35 is pathway associated with overexpression of argininosuccinate synthase (ASS1) and arginosuccinate ly
36 or miR-1291) may modulate the expression of argininosuccinate synthase (ASS1) and glucose transporte
40 , CLOCK directly acetylates K165 and K176 of argininosuccinate synthase (ASS1) to inactivate ASS1, wh
41 , we identify the epigenetic reactivation of argininosuccinate synthase (ASS1), a urea cycle enzyme s
43 gen efflux by upregulating the expression of argininosuccinate synthase 1 (ASS1), a key enzyme in the
44 Multiple KSHV-encoded microRNAs upregulate argininosuccinate synthase 1 (ASS1), a key enzyme in the
45 els for phosphoenolpyruvate carboxykinase 1, argininosuccinate synthase 1, sodium/glucose co-transpor
46 es in the arginine-recycling pathway enzymes argininosuccinate synthase and ornithine transcarbamylas
47 0461) of H. influenzae, the gene encoding an argininosuccinate synthase homolog, and a change in the
48 ucocorticoid-induced leucine zipper protein, argininosuccinate synthase, and human prostaglandin tran
49 ven up-regulated proteins were identified as argininosuccinate synthase, argininosuccinate lyase, neu
50 e (AUC) for cytoplasmic aconitate hydratase, argininosuccinate synthase, carbamoylphosphate synthase,
51 also inhibited cytokine induction in CMEC of argininosuccinate synthase, the rate-limiting enzyme for
53 ic carcinoma cells through the regulation of argininosuccinate synthase- and glucose transporter prot
54 quires the sequential action of two enzymes, argininosuccinate synthetase (AS) and argininosuccinate
55 anomas and other cancers that do not express argininosuccinate synthetase (AS), the rate-limiting enz
58 ted urea cycle disorder that is caused by an argininosuccinate synthetase (ASS) enzyme deficiency.
59 gh energy demand, the ornithine cycle enzyme argininosuccinate synthetase (ASS) is a principle site o
60 nous arginine is required for growth in some argininosuccinate synthetase (ASS)-deficient cancers.
61 two-hybrid screening of PRMT7 and identified argininosuccinate synthetase (ASS1) as a potential inter
63 ed to influence HSV-1 replication, including argininosuccinate synthetase 1 (AS1), which consumes asp
64 20) depletes essential amino acid levels in argininosuccinate synthetase 1 (ASS1) -negative tumors b
65 s study, we focused on the urea cycle enzyme argininosuccinate synthetase 1 (ASS1) as a therapeutic t
69 inine deprivation is synthetically lethal in argininosuccinate synthetase 1 (ASS1)-negative cancers,
73 ot only enhanced the cellular sensitivity of argininosuccinate synthetase 1-positive GBM to ionizing
74 synthesized from citrulline in two steps by argininosuccinate synthetase and argininosuccinate lyase
75 he citrulline to arginine converting enzymes argininosuccinate synthetase and argininosuccinate lyase
76 le metabolism characterized by deficiency of argininosuccinate synthetase and consequent life-threate
79 uished asymptomatic heterozygous carriers of argininosuccinate synthetase deficiency (0.22 +/- 0.03),
81 of melanoma and HCC is due to the absence of argininosuccinate synthetase in these cells and that an
84 1-deleted adenoviral vector expressing human argininosuccinate synthetase resulted in transduction of
86 loid leukemias (AMLs) have low expression of argininosuccinate synthetase-1 (ASS1), rendering AML cel