1 in humans include APOC3, lipoprotein lipase, sphingomyelin phosphodiesterase 1, and glucocerebrosidas

2 n by VSMCs, most likely by the activation of sphingomyelin phosphodiesterase 3 (SMPD3) and cytoskelet

3 on functionally characterizing 2 candidates, sphingomyelin phosphodiesterase 3 (SMPD3) and neurofilam

4                                              Sphingomyelin phosphodiesterase 3 (SMPD3), a lipid-metab

5 ed extracellular calcium was found to induce sphingomyelin phosphodiesterase 3 expression and the sec

6 m VSMCs in vitro, and chemical inhibition of sphingomyelin phosphodiesterase 3 prevented VSMC calcifi

7 and CD81, and their release was regulated by sphingomyelin phosphodiesterase 3.

8                   This screen identified the sphingomyelin phosphodiesterase acid-like 3A (SMPDL3A) g

9 phages that showed that transcription of the sphingomyelin phosphodiesterase acid-like 3A (SMPDL3A) g

10 proteinuria possibly associated with loss of sphingomyelin phosphodiesterase acid-like 3b (SMPDL-3b).

11                  The lipid-modulating enzyme sphingomyelin phosphodiesterase acid-like 3B (SMPDL3b) i

12                                              Sphingomyelin phosphodiesterase, acid-like 3A (SMPDL3A)

13                  Acid sphingomyelinase (ASM; sphingomyelin phosphodiesterase, EC 3.1.4.12) is the lys

14  Neutral sphingomyelinase SMPD3 (nSMase2), a sphingomyelin phosphodiesterase, resides in the Golgi ap

15            Sphingomyelin synthases (SMS) and sphingomyelin phosphodiesterase (SMase) enzymes may play

16 sphatidylcholine acyltransferase (LPCAT) and sphingomyelin phosphodiesterase (SMPD) expression.