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Transmembrane Signaling through Voltage-gated Ca Channel

Transmembrane Signaling through Voltage-gated Ca Channel
通过电压门控 Ca 通道的跨膜信号传导
批准号:
7007548
负责人:
Lutz Birnbaumer
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

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中文摘要
翻译
研究了通道内口(S6结构域末端)丝氨酸的重要性。它的丙氨酸突变取消了通道在激活PKA或添加BAY-K8644的刺激下进入模式2门控的能力。丝氨酸(Ser 1517)可能是一个关键的调控位点,它与先前研究的选择性过滤器中的Ser 1142协同决定通道对磷酸化和二氢吡啶激动剂的响应。我们正在测试一种假设,即模式2门通的损失是由于Ser 1517和附近的两个赖氨酸中的一个之间建立了一个离子桥,从而“冻结”了。处于模式1门控的通道。
英文摘要
The importance of a serine at the inner mouth of the channel (end of domain IV S6 segment) was studied. Its mutation to alanine abrogated the ability of the channel to enter into mode 2 gating upon stimulation by activation of PKA or addition of BAY-K8644. The serine (Ser 1517) may be a key regulatory site that determines, in coordination with the previously studied Ser 1142 in the selectivity filter, the responsivenes of the channel to phosphorylation and the dihydropyridine agonist. We are testing the hypothesis that loss of mode 2 gating is due to establshment of an ionic bridge between Ser 1517 and one of two nearby lysines from domain I, thus ?freezing? the channel in mode 1 gating.
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3D RENDITION/QUANTITATIVE ANALYSIS GI2 DEFICIENT MICE
  • 批准号:
    7358258
  • 项目类别:
  • 资助金额:
    $2.05万
  • 财政年份:
    2006
  • 负责人:
    Lutz Birnbaumer
  • 依托单位:
3D RENDITION/QUANTITATIVE ANALYSIS GI2 DEFICIENT MICE
  • 批准号:
    7181529
  • 项目类别:
  • 资助金额:
    $2.13万
  • 财政年份:
    2005
  • 负责人:
    Lutz Birnbaumer
  • 依托单位:
3D RENDITION/QUANTITATIVE ANALYSIS GI2 DEFICIENT MICE
  • 批准号:
    6977825
  • 项目类别:
  • 资助金额:
    $2.8万
  • 财政年份:
    2004
  • 负责人:
    Lutz Birnbaumer
  • 依托单位:
CORE--MOLECULAR PROBES
  • 批准号:
    6594231
  • 项目类别:
  • 资助金额:
    $17.42万
  • 财政年份:
    2002
  • 负责人:
    Lutz Birnbaumer
  • 依托单位:
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