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2 in humans include APOC3, lipoprotein lipase, sphingomyelin phosphodiesterase 1, and glucocerebrosidas
3 n by VSMCs, most likely by the activation of sphingomyelin phosphodiesterase 3 (SMPD3) and cytoskelet
4 on functionally characterizing 2 candidates, sphingomyelin phosphodiesterase 3 (SMPD3) and neurofilam
6 y, AMPKalpha promotes the phosphorylation of sphingomyelin phosphodiesterase 3 (SMPD3), stabilizing t
7 ed extracellular calcium was found to induce sphingomyelin phosphodiesterase 3 expression and the sec
8 m VSMCs in vitro, and chemical inhibition of sphingomyelin phosphodiesterase 3 prevented VSMC calcifi
9 enetic marginal effects, aside from 16q22.1 (sphingomyelin phosphodiesterase 3, or SMPD3) and 19q13.2
11 phages that showed that transcription of the sphingomyelin phosphodiesterase acid-like 3A (SMPDL3A) g
13 proteinuria possibly associated with loss of sphingomyelin phosphodiesterase acid-like 3b (SMPDL-3b).
14 sphingolipids and the lipid-modifying enzyme sphingomyelin phosphodiesterase acid-like 3b (SMPDL3b) i
17 a novel role for the lipid-modifying enzyme, sphingomyelin phosphodiesterase acid-like 3b (SMPDL3b),
21 Neutral sphingomyelinase SMPD3 (nSMase2), a sphingomyelin phosphodiesterase, resides in the Golgi ap