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1 MA) and symmetrically dimethylated arginine (SDMA).
2 (ADMA), but not symmetric dimethylarginine (SDMA).
3 tivity] and with symmetric dimethylarginine (SDMA).
4 inine (ADMA) and symmetric dimethylarginine (SDMA).
5 es form symmetrically dimethylated arginine (SDMA).
6 thylarginine and symmetric dimethylarginine (SDMA).
7 of proteins with symmetric dimethylarginine (sDMA).
8 site enables PRMT1 to generate both ADMA and SDMA.
9 ividual variability in ADMA, l-arginine, and SDMA.
10 itive independent associations with ADMA and SDMA.
11 nical THW loop enables the enzyme to produce SDMA.
12 FSR inversely correlated with both ADMA and SDMA.
13 ake into the cell (ADMA and symmetrical DMA [SDMA]).
15 sociation between increased plasma levels of SDMA, AGXT2 variants, and various cardiometabolic risk f
20 arginine (ADMA), symmetric dimethylarginine (SDMA), and N-monomethylarginine (MMA) were quantified at
21 AGXT2) regulates systemic levels of ADMA and SDMA, and also of beta-aminoisobutyric acid (BAIB)-a mod
23 ginine (ADMA) and symmetric dimethyarginine (SDMA) are independent mortality predictors in atheroscle
24 ts stereo-isomer symmetric dimethylarginine (SDMA), are increased in alcoholic hepatitis patients, an
26 ts the levels of symmetric dimethylarginine (SDMA) at Arg-3 on histone H4, leading to the repression
28 essed serum levels of homoarginine, ADMA and SDMA by LC-MS/MS in 865 individuals from a prospective c
29 ine, ADMA, and symmetrical dimethylarginine (SDMA) by high-performance liquid chromatography in 49 hy
33 inine (ADMA) and symmetric dimethylarginine (SDMA) concentrations in conditions reportedly associated
34 gest that PIWI family member SMEDWI-3 is one sDMA-containing chromatoid body protein for which methyl
35 atic reduction of the steady-state levels of sDMA-containing proteins in MTAP+ cells, even though no
37 s indicate that the higher energy barrier of SDMA formation (DeltaDeltaG(double dagger) = 3.2 kcal/mo
40 tudy reveals unique energetic challenges for SDMA-forming methyltransferases and highlights the exqui
41 also support emerging studies indicative of sDMA function in stabilization of RNP granules and the P
44 emoglobin, ADMA, symmetric-dimethylarginine (SDMA), histidine-rich protein-2, and angiopoietin-2 were
45 ic and symmetric dimethylarginines (ADMA and SDMA) impair nitric oxide bioavailability and have been
47 r data demonstrate a role for PRMT5-mediated SDMA in the context of RS-induced transcriptional induct
50 nine and high circulating levels of ADMA and SDMA independently predict all-cause mortality in patien
51 s of homoarginine and high levels of ADMA or SDMA independently predicted all-cause mortality after a
52 zed as a cardiovascular risk marker, whereas SDMA is a novel marker for renal function and associated
53 e formation of symmetrical dimethylarginine (sDMA), is a nucleolin-associated protein whose localizat
54 exposure, C-reactive protein, serum ADMA and SDMA (LC-MS/MS), and thiols (homocysteine, cysteine, tau
56 ated glomerular filtration rate, an elevated SDMA-level (4th quartile, >1.38 mumol/L) was associated
60 ltered levels of PRMT5 activity (assessed by sDMA levels) in accord with changes in its localization.
61 there are major increases in global MMA and SDMA levels, as detected by type-specific antibodies.
65 vivo evidence demonstrating that Sm protein sDMA modification is required for snRNP biogenesis in hu
66 ation, whereas ubiquitous expression rescues sDMA modification of Sm proteins and male sterility.
72 irectly to the symmetrical dimethylarginine (sDMA)-modified arginine- and glycine-rich (RG-rich) doma
74 dart5 and valois causes the specific loss of sDMA-modified Sm proteins and studies in C. elegans show
75 We found that the unmodified, but not the sDMA-modified, RG domains of SmD1 and SmD3 associate wit
76 al modification, symmetric dimethylarginine (sDMA), of Aub is essential for piRNA biogenesis, transpo
77 he presence of symmetrical dimethylarginine (sDMA) on chromatoid body components and identify the ort
78 rst analysis, whether homoarginine, ADMA and SDMA predict venous thromboembolism (VTE) recurrence and
79 ic and symmetric dimethylarginines (ADMA and SDMA) predict and potentially contribute to end organ da
80 er asymmetric or symmetric dimethylarginine (SDMA), PRMT7 is unique in producing solely monomethylarg
81 inine (ADMA) and symmetric dimethlyarginine (SDMA) ratio (OR per 1 SD, 1.19; 95% CI: 1.02-1.41), N1-a
88 broblasts results in almost complete loss of SDMA, suggesting that PRMT5 is the primary SDMA-forming