張海林[河北醫科大學院長]

張海林,1960年12月出生,中共黨員,1984年畢業於河北醫科大學醫學專業,獲學士學位;1987年在獲河北醫科大學藥理學碩士學位;1995年在英國倫敦大學聖喬治醫學院(St. George’s Hospital Medical School)藥理系獲博士學位。曾先後在英國倫敦大學、美國霍華德休斯醫學研究所(Howard Hughes Medical Institute)、美國紐約大學西奈山醫學中心(Mount Sinai Medical Center)進行博士後研究,2000年起任職於西奈山醫學中心生理與生物物理系。2001年10月以特殊人才受聘於河北醫科大學。現為河北醫科大學藥理教研室教授,燕趙學者,博士生導師,基礎醫學院院長,基礎醫學研究所藥理研究室主任,基礎醫學院藥理教研室副主任。主要從事離子通道的結構與功能關係、細胞信號傳導及對離子通道的調節機制研究。已在包括《Nature Cell Biology》, 《Neuron》, 《Nature Neuroscience》, 《EMBO》, 《J. Biol. Chem.》等國際專業雜誌上發表科研究論文多篇。燕趙學者,獲國家傑出青年科學基金,並主持美國國家衛生研究院(NIH)國際合作基金項目、科技部重大基礎研究前期研究專項、國家自然科學基金、教育部重點項目等。2005年河北省十大科技傑出青年獲得者。

個人簡介

學位:博士

職務:河北醫科大學基礎醫學院院長,基礎醫學研究所藥理研究室主任

研究方向:

內向整流鉀離子通道的結構與功能

信號傳導的分子機制

離子通道功能的調節

分子生理學,分子藥理學及神經生物學

成就

燕趙學者,國家傑出青年科學基金獲得者,享受國務院政府特殊津貼,獲中國僑聯科技創新人才獎,河北省十大科技傑出青年,河北省強勢學科(藥理學)帶頭人,省管優秀專家。中國僑聯特聘專家。主持國家自然科學基金傑出青年科學基金項目、重點項目、面上項目、國際合作項目;國家973課題、國家863計畫、科技部重大基礎研究前期研究專項;美國國家衛生研究院(NIH)國際合作基金項目等。在國際高水平的學術雜誌《Nature Cell Biology》等發表SCI論文60多篇;研究成果獲河北省自然科學一等獎。

重要學術論文

1. Peng LY, Mirshahi T., Zhang HL., Hirsch J. and Logothetis DE (2003) Critical Determinants of the G Protein g Subunits in the Gbg Stimulation of G Protein-actiated Inwardly Rectifying Potassium (GIRK) Channel Actiity. J Biol Chem 278 (50), 50203–50211,

2. Chan KW, Zhang HL and Logothetis1 DL (2003) N-terminal transmembrane domain of the SUR controls trafficking and gating of Kir6 channel subunits. The EMBO Journal, 22 (15) 3833-3843

3. Zhang H., Craciun LC, Mirshahi T, Rohács T, Lopes CMB, Jin T, and Logothetis DE. (2003) PIP2 Actiates KCNQ Channels, and Its Hydrolysis Underlies Receptor-Mediated Inhibition of M Currents. Neuron, 37(6), 963-975

4. Lopes C M.B., Zhang H., Rohacs T, Jin T, Yang, J. and Logothetis D.E. (2002) Alterations in Consered Kir Channel-PIP2 Interactions Underlie Channelopathies. Neuron, 34, 933–944

5. Perez CA., Huang L., Rong M., Kozak JA., Zhang H., Max M. and Margolskee RF. (2002). A transient receptor potential channel expressed in taste receptor cells. Nature Neurosci. 5(11):1169-76.

6. Mirshahi T, Mittal , Zhang H, Linder ME, Logothetis DE. (2002) Distinct sites on G protein beta gamma subunits regulate different effector functions. J Biol Chem 277(39):36345-50.

7. He C, Yan X, Zhang H, Mirshahi T, Jin T, Huang A, Logothetis DE (2002) Identification of critical residues controlling G protein-gated inwardly rectifying K(+) channel actiity through interactions with the beta gamma subunits of G proteins. J Biol Chem 277:6088-96

8. Mirshahi T, Robillard L, Zhang H, Hebert TE, Logothetis DE (2002) Gbeta residues that do not interact with Galpha underlie agonist-independent actiity of K+ channels. J Biol Chem 277(9):7348-55

9. Rohac T., Lopes CMB., Mirshahi T., Jin T., Zhang H. & Logothetis DE. (2001). Assay pf phosphatidylinositol biphosphate regulation of potassium channels. In G protein pathways, part C: Effector mechanism. Methods in Enzymology, 345-357

10. Hughes TE, Zhang, HL, Logothetis DE, Berlot CH (2001). isualization of a functional Gaq-green fluorescent protein fusion in liing cells: Association with the plasma membrane is disrupted by mutational actiation and by elimination of palmitoylation sites, but not by actiation mediated by receptors or AlF4- . J Biol Chem, 276:4227-4235.

11. Kobrinsky E, Mirshahi T, Zhang H, Jin T, Logothetis DE (2000). Receptor-mediated hydrolysis of plasma membrane messenger PIP2 leads to K+-current desensitization. Nature Cell Biology, 2:507-14.

12. Zhang,HL., He C., Yan XX, Mirshahi T and Logothetis DE. (1999) Actiation of inwardly rectifying K+ channels by distinct PtdIns(4,5)P2 interactions. Nature Cell Biology, 1:183-188

13. He, C., Zhang, HL., Mirshahi, T. and Logothetis, D. (1999). Specific Gbg Interaction With a K+ Channel Distinguish Between Basal and Agonist-induced Currents. J. Bio. Chem, 274:12517-12524

14. Logothetis, E.D. & Zhang, HL. (1999) Gating of G protein-sensitie inwardly rectifying K+ channels through phosphatidylinositol 4,5-bisphosphate-dependent mechanism. J. Physiol. London, 520, 630

15. Zhang, H-L., T. B. Bolton, A. E. Piekarska & G. A. McPherson (1998). The electrophysiological effects of tetraphenylphosphonium and tetraphylboron on ascular somooth muscle. Eur. J. Pharmacol, 347(1), 119-23

16. Zhang, H-L & Bolton, T. B. (1996) ATP-sensitie potassium channels and their modulation by nucleotides and potassium channel openers in ascular smooth muscle cells. In: Smooth muscle excitation. Eds: Bolton T. B. & Tomita, T. Academic Press Limited. Chapter 12, pp 139-154

17. Zhang, H-L. & Bolton, T. B. (1996). Two types of ATP-sensitie potassium channels in rat portal ein smooth muscle cells. Br. J. Pharmacol. 118, 105-114

18. Zhang, H-L. & Bolton, T. B. (1995). Effects of UK-84149 on oltage-actiated calcium currents of single smooth muscle cells from guinea-pig and rabbit jejunum and rabbit coronary. Br. J. Pharmacol., 114, 1657-1665

19. Zhang, H-L. & Bolton, T. B. (1995). Actiation by Intracellular GDP, metabolic inhibition and pinacidil of a glibenclamide-sensitie K-channel in smoothmuscle cells of rat mesenteric artery. Br. J. Pharmacol., 114, 662-672

20. Beech, D.J., Zhang, H., Nakao, K. & Bolton, T.B. (1993). Single channel and whole-cell K-currents eoked by lecromakalim in smooth muscle cells from the rabbit portal ein. Br. J. Pharmacol., 110, 583-590.

21. Beech, D.J., Zhang, H., Nakao, K. & Bolton, T.B. (1993). K channel actiation by nucleotide diphosphates and its inhibition by glibenclamide in ascular smooth muscle cells. Br. J. Pharmacol., 110, 573-582

著作

A text book of fundamental medical pharmacology (英文), 編委,吉林科學技術出版社, 2004

承擔課題

1. 國家傑出青年科學基金 (30325038), 2004.1-2007.12

2. 美國國家衛生研究院NIH Fogarty 國際合作項目(1 R03 TW006020-01A1): Protein Kinase C-dependent inhibition of Kir channels, 2003.4-2006.4,

3. 科技部基礎研究重大項目前期研究專項(2003CCA00300):細胞膜磷脂對離子通道功能的調節及其生理學意義, 2003.12-2005.12

4. 國家自然科學基金項目(30270361): 膜磷脂PIP2對M電流及KCNQ電流的調節作用. 2003.1-2005.12,

5. 河北省自然科學基金項目。磷脂醯肌醇二磷酸對M電流的調節及生理學意義(303464),2003.1-2005.12

6. 國家自然科學基金項目(30240001): 老年大鼠M電流的研究. 2002.1---2002.12,

7. 教育部科學技術研究重點項目(02016): pH調節內向整流鉀離子通道功能的分子機制, 2002.1-2003.12

最近完成的工作主要是有關膜磷脂PIP2在調節鉀離子通道功能作用方面的研究,主要包括以下幾個部分:(1)提出並證明了PIP2可作為生理性調節的、影響鉀離子通道的直接信號分子這一新的概念。(2)提出並證明了鉀離子通道中胺基酸突變所造成的通道蛋白-PIP2分子間反應的改變是導致遺傳性疾病Andersen 綜合症及Barters綜合症的分子基礎;(3)證明PIP2對於維持神經細胞M電流和KCNQ通道的功能至關重要,而神經遞質誘發M電流和KCNQ通道抑制的機制是由於它們共有的導致PIP2水解所為;(4)提出並證明了通道蛋白-PIP2反應特徵決定了pH、PKC、Mg2+ 等調節Kir鉀通道的特徵,提出了通道蛋白-PIP2反應可能是決定各種調節因素調節通道功能的共有的關鍵機制的新觀點。

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