MARCKS phosphorylation and amylase release in GLP-1-stimulated acini isolated from rat pancreas
MARCKS phosphorylation and amylase release in GLP-1-stimulated acini isolated from rat pancreas
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从大鼠胰腺中分离出 GLP-1 刺激的腺泡中的 MARCKS 磷酸化和淀粉酶释放
DOI：
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发表时间：
2018
影响因子：
2.3
通讯作者：
M. Kashimata
中科院分区：
文献类型：
--
作者：
Keitaro Satoh;M. Ouchi;Asuka Morita;M. Kashimata
胰高血糖素样肽1（GLP-1）对胰腺外分泌腺的影响知之甚少。在腺体中，促分泌素诱导淀粉酶释放。该信号转导主要由细胞内Ca 2+水平的增加和蛋白激酶C（PKC）的活化引起。我们以前证明，豆蔻酰丙氨酸丰富的C激酶底物（MARCKS），PKC底物，参与胰腺淀粉酶的释放。在此，我们研究了GLP-1对大鼠胰腺腺泡中MARCKS磷酸化和淀粉酶释放的影响。GLP-1诱导分离胰腺腺泡中淀粉酶释放和MARCKS磷酸化。cAMP依赖性蛋白激酶（PKA）抑制剂抑制了这些作用。此外，MARCKS相关肽抑制GLP-1诱导的淀粉酶释放。这些发现表明，GLP-1诱导淀粉酶释放通过MARCKS磷酸化通过激活PKA在分离的胰腺腺泡。
Little is known about the effects of glucagon-like peptide 1 (GLP-1) on the pancreatic exocrine gland. In the gland, secretagogues induce amylase release. That signal transduction is evoked mainly by an increase in intracellular Ca2+ levels and activation of protein kinase C (PKC). We previously demonstrated that myristoylated alanine-rich C kinase substrate (MARCKS), a PKC substrate, is involved in pancreatic amylase release. Here, we studied the effects of GLP-1 on MARCKS phosphorylation and amylase release in rat pancreatic acini. GLP-1 induced amylase release and MARCKS phosphorylation in isolated pancreatic acini. Inhibitors of cAMP-dependent protein kinase (PKA) suppressed those effects. Furthermore, a MARCKS-related peptide inhibited the GLP-1-induced amylase release. These findings suggest that GLP-1 induces amylase release through MARCKS phosphorylation via activation of PKA in isolated pancreatic acini.
DOI：
10.1073/pnas.86.11.4012
发表时间：
1989-06
影响因子：
11.1
作者：
D. Stumpo;Jonathan M. Graff;Katherine A. Albert;Paul Greengard;P. J. Blackshear
通讯作者：
D. Stumpo;Jonathan M. Graff;Katherine A. Albert;Paul Greengard;P. J. Blackshear
胆囊收缩素刺激的离体大鼠胰腺腺泡中 1,2-二酰基甘油的多种来源。
DOI：
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发表时间：
1989
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Matozaki,T;Williams,JA
通讯作者：
Williams,JA
DOI：
10.1152/ajpgi.00293.2015
发表时间：
2016-01-01
影响因子：
4.5
作者：
Hou, Yanan;Ernst, Stephen A.;Williams, John A.
通讯作者：
Williams, John A.