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  1. 020 学位論文
  2. 生命科学研究科
  3. 20 生理科学専攻

Regulation of volume-sensitive chloride channels by cystic fibrosis transmembrane conductance regulator and epidermal growth factor receptor

https://ir.soken.ac.jp/records/1124
https://ir.soken.ac.jp/records/1124
edace3b8-c90c-4ccf-b643-6f3ff4a3c0d9
名前 / ファイル ライセンス アクション
甲620_要旨.pdf 要旨・審査要旨 / Abstract, Screening Result (208.6 kB)
甲620_本文.pdf 本文 (2.6 MB)
Item type 学位論文 / Thesis or Dissertation(1)
公開日 2010-02-22
タイトル
タイトル Regulation of volume-sensitive chloride channels by cystic fibrosis transmembrane conductance regulator and epidermal growth factor receptor
タイトル
タイトル Regulation of volume-sensitive chloride channels by cystic fibrosis transmembrane conductance regulator and epidermal growth factor receptor
言語 en
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_46ec
資源タイプ thesis
著者名 ABDULLAEV, Iskandar Fatkhullaevich

× ABDULLAEV, Iskandar Fatkhullaevich

ABDULLAEV, Iskandar Fatkhullaevich

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フリガナ アブデルブ, イシカンダル

× アブデルブ, イシカンダル

アブデルブ, イシカンダル

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著者 ABDULLAEV, Iskandar Fatkhullaevich

× ABDULLAEV, Iskandar Fatkhullaevich

en ABDULLAEV, Iskandar Fatkhullaevich

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学位授与機関
学位授与機関名 総合研究大学院大学
学位名
学位名 博士(理学)
学位記番号
内容記述タイプ Other
内容記述 総研大甲第620号
研究科
値 生命科学研究科
専攻
値 20 生理科学専攻
学位授与年月日
学位授与年月日 2002-03-22
学位授与年度
値 2001
要旨
内容記述タイプ Other
内容記述 Effectene-mediated transient expression of wild-type (WT) human cystic fibrosis transmembrane conductance regulator (CFTR) in HEK293T cells resulted in a 3- times decrease of the amplitude of steady-state volume-sensitive outwardly rectifying (VSOR) chloride current, Expression of the CFTR ΔF508 mutant, which cannot be translocated to the plasma membrane, failed to mimic the CFTR effect on the VSOR Cl- current, suggesting that plasma membrane expression of CFTR protein is necessary for its regulatory effect on the VSOR Cl- channel. Expression of the G1349D mutant of CFTR, which impairs ATP binding to the NBD2 domain of CFTR protein, failed to inhibit VSOR Cl- currents.D1370N and K1250M mutations in NBD2 domain, which impair ATP hydrolysis, were also ineffective in down-regulating VSOR C1-currents.In contrast, expression of G551D mutant, which impairs ATP binding to the NBDl domain, mimicked the effect of WT- CFTR.Thus, I conclude that plasma membrane expression of an ATP- hydrolysable conformation of the NBD2 domain of CFTR is essential for its down-regulatory action on the volume-sensitive chloride conductance in HEK293T/CFTR cells.<br /><br />In mouse mammary gland C127 cells, in contrast, VSOR Cl- currents were up- regulated by stable expression of CFTR mediated by bovine papillomavirus (BPV), a carrier for CFTR gene transfection, by around 3-fold.Also, BPV- mediated expression with CFTR ΔF508 mutant produced a similar up-regulating effect on VSOR Cl- currents.BPV expression is known to constitutively activate receptors to platelet-derived growth factor (PDGF) and epidermal growth factor (EGF).Application of a PDGF peptide or a specific inhibitor of PDGF tyrosine kinase, tyrphostin AGl296, had no effect on VSOR Cl-currents.In contrast, application of an EGF peptide enhanced VSOR Cl-currents in Cl27 cells, but not in Cl27 cells treated with BPV(Cl27/BPV cells).A specific inhibitor of EGF- receptor tyrosine kinase, tyrphostin B46, profoundly suppressed VSOR Cl-currents in Cl27 and Cl27/BPV cells.Thus, I conclude that VSOR Cl-channels are enhanced by an EGF receptor tyrosine kinase signaling and that BPV-induced up-regulation overrides CFTR-induced down-regulation of VSOR Cl-channels in Cl27/CFTR cells.Since inhibitors of phospholipase Cγ(PLCγ), phosphatidylinositol-3-kinase (PI3K) and MAP kinase kinase (MEK) failed to affect the VSOR Cl-channel activity, it might be possible that the VSOR Cl- channel is regulated by some signaling pathway, other than those involving PLCγ,PI3K and MEK, which is downstream to the EGF receptor tyrosine kinase.
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内容記述 application/pdf
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