Calcium transport pathways of pancreatic acinar cells.
Calcium transport pathways of pancreatic acinar cells.
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胰腺腺泡细胞的钙转运途径。
DOI：
10.1146/annurev.ph.51.030189.000503
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发表时间：
1989
影响因子：
18.2
通讯作者：
Muallem,S
中科院分区：
文献类型：
--
作者：
Muallem,S
在静息和刺激的胰腺腺泡细胞中，[Ca 2 +] i的控制通过至少四种Ca 2+转运途径来实现。细胞质膜和内质网膜中的传导通路允许Ca 2+流入胞质溶胶，而ATP驱动的Ca 2+泵从胞质溶胶中除去Ca 2+。这些Ca 2+途径对胞质Ca 2+的贡献如图2所示。在静息细胞中，[Ca 2 +] i由Ca 2+跨质膜流入和流出的速率决定。将胞质Ca 2+缓冲至约150 nM。Ca 2+泵送穿过质膜的速率等于Ca 2+内流的速率，这使[Ca 2 +] i保持在恒定水平。细胞质Ca 2+的缓冲防止[Ca 2 +] i的大幅波动。ER含有约3纳摩尔钙/mg细胞蛋白。ER钙可能也被缓冲，这导致ER内部的游离Ca 2+浓度较低。ER膜的Ca 2+渗透性非常低。低ER游离Ca 2+浓度和Ca 2+渗透性导致ER Ca 2+泵的Ca 2+泵送速率低。Ca 2+穿过ER膜的低泵漏周转率使ER对静息细胞中[Ca 2 +] i的贡献最小化。当细胞受到刺激时，一系列事件开始，其最终结果是[Ca 2 +] i的瞬时增加。为了产生[Ca 2 +] i的瞬时增加，改变了四种Ca 2+途径的活性。每个Ca 2+通路的激活顺序尚未完全解决。然而，激动剂与受体结合后可能会激活磷脂酶C（PLC）。PLC催化PIP 2分解为IP 3和甘油二酯（DAG）。在随后的刺激周期中，PIP 2也水解为IcP 3。在刺激开始时，ER中的Ca 2+缓冲液的性质可能会改变，使得ER内部的游离Ca 2+浓度增加。IP 3与ER膜中的特异性受体结合并激活Ca 2+传导。这导致Ca 2+从ER流出到胞质溶胶，并且K+通过K+传导途径从胞质溶胶流入到ER。尚不清楚K+流入是否足以平衡作为Ca 2+释放的电荷。在肌肉SR的情况下，建议需要K+、Mg 2+和H+流入来平衡以Ca 2+形式释放的电荷（110）。（250字处删节）
The control of [Ca2+] i in resting and stimulated pancreatic acinar cells is achieved by at least four Ca2+ transporting pathways. Conductive pathways in the plasma and ER membranes allow Ca2+ influx into the cytosol while ATP-fueled Ca2+ pumps remove Ca2+ from the cytosol. The contribution of these Ca2+ pathways to cytosolic Ca2+ is illustrated in the Figure 2. In the resting cells,[Ca2+] i is determined by the rates of Ca2+ influx and efflux across the plasma membrane. Cytosolic Ca2+ is buffered to approximately 150 nM. The rate of Ca2+ pumping across the plasma membrane is equal to the rate of Ca2+ influx, which keeps [Ca2+] i at a constant level. The buffering of cytosolic Ca2+ prevents large fluctuations in [Ca2+] i. The ER contains about 3 nmoles calcium/mg of cell protein. ER calcium is probably also buffered, which results in low free Ca2+ concentration in the ER interior. The Ca2+ permeability of the ER membrane is very low. The low ER free Ca2+ concentration and Ca2+ permeability result in a low rate of Ca2+ pumping by the ER Ca2+ pump. The low pump-leak turnover rate of Ca2+ across the ER membrane minimizes the contribution of the ER to [Ca2+] i in the resting cells. When the cells are stimulated, a sequence of events is initiated, the end result of which is a transient increase in [Ca2+] i. To produce the transient increase in [Ca2+] i, the activity of the four Ca2+ pathways is modified. The sequence of activation of each Ca2+ pathway has not been completely resolved. It is, however, likely that binding of agonist to a receptor is followed by activation of phospholipase C (PLC). PLC catalizes the breakdown of PIP2 to IP3 and diacylglycerol (DAG). In subsequent stimulation periods PIP2 is also hydrolyzed to IcP3. At the onset of stimulation, the properties of the Ca2+ buffer in the ER may be changed so that free Ca2+ concentration in the ER interior is increased. IP3 binds to specific receptors in the ER membrane and activates a Ca2+ conductance. This leads to Ca2+ efflux from the ER to the cytosol and K+ influx from the cytosol to the ER through a K+ conductive pathway. It is unclear if K+ influx is sufficient to balance the charge released as Ca2+. In the case of muscle SR, it was suggested that K+, Mg2+, and H+ influx are required to balance the charge released as Ca2+(110).(ABSTRACT TRUNCATED AT 250 WORDS)
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影响因子：
5.5
作者：
CASE, RM;CLAUSEN, T
通讯作者：
CLAUSEN, T
大鼠胰腺腺泡细胞胞质游离 Ca2+ 浓度的调节。
影响因子：
--
作者：
H. Streb;I. Schulz
通讯作者：
I. Schulz
凝血酶或佛波醇肉豆蔻酸酯乙酸酯激活的装载 fura-2 的血小板刺激 Ca2+ 流出
影响因子：
3.5
作者：
W. K. Pollock;S. Sage;T. Rink
通讯作者：
T. Rink
用氨甲酰胆碱刺激小鼠胰腺小叶时形成肌醇 1,2-环 4,5-三磷酸和肌醇 1,2-环 4-二磷酸。
DOI：
--
发表时间：
1987
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Sekar,MC;Dixon,JF;Hokin,LE
通讯作者：
Hokin,LE
人血小板膜中的 Ca2 转运。
影响因子：
4.8
作者：
S. Adunyah;W. Dean
通讯作者：
W. Dean