發(fā)布時間：2018-09-19 20:12

【摘要】： G蛋白偶聯(lián)受體(GPCR)是目前已發(fā)現(xiàn)受體中種類最多的一類。這些受體在結(jié)構(gòu)上有很大的相似性,由一條肽鏈形成,跨膜七次,N端在胞外,C端在胞內(nèi)。這些受體與效應(yīng)器間都通過G蛋白介導(dǎo)。G蛋白種類較多,但所有類型G蛋白都由3個不同的亞單位即α、β、γ所組成,α亞單位具有特異的GTP結(jié)合位點(diǎn),有GTP酶活性。根據(jù)G蛋白的α亞單位的結(jié)構(gòu),可將其分為6個亞家族:Gs,Gi/o,Gq,Gt,Gg和G12[1]。由Gq蛋白偶聯(lián)受體介導(dǎo)的磷脂酶C (PLC)信號系統(tǒng)是一種廣泛存在的信號轉(zhuǎn)導(dǎo)機(jī)制。Gαq蛋白激活后首先激活PLCβ,進(jìn)而水解胞膜PIP2,水解生成兩種第二信使IP3與DAG,進(jìn)而調(diào)控諸多細(xì)胞功能,例如離子通道功能、細(xì)胞周期、腺體分泌,等等。 IP3受體廣泛存在于細(xì)胞內(nèi)質(zhì)網(wǎng)膜上,它是一種能引發(fā)內(nèi)鈣釋放的通道蛋白,能與IP3結(jié)合,引發(fā)細(xì)胞內(nèi)鈣釋放,導(dǎo)致內(nèi)鈣水平的升高,從而啟動細(xì)胞內(nèi)鈣信號系統(tǒng),通過依賴鈣離子的鈣調(diào)素等酶類活性的變化來調(diào)控一系列的生理過程。到目前為止,共有四種IP3受體被發(fā)現(xiàn),其中,Ⅰ型受體廣泛存在于神經(jīng)組織中。細(xì)胞內(nèi)鈣的釋放在細(xì)胞信號轉(zhuǎn)導(dǎo)過程中具有重要的作用。另外,鈣信號的異常也參與了諸多病理過程中。 M電流是在1980年由Brown和Admas在牛蛙的頸上交感神經(jīng)節(jié)被首次發(fā)現(xiàn),它是一種慢激活,非失活的電壓依賴性外向鉀離子電流,因其可被毒蕈堿受體強(qiáng)烈抑制而得名。自1998年以來人們逐漸認(rèn)識到其分子基礎(chǔ)是KCNQ家族(KCNQ2/3)的鉀離子通道。M電流與神經(jīng)系統(tǒng)的興奮性密切相關(guān)。自電流被發(fā)現(xiàn)到現(xiàn)在20多年的時間里,人們對其調(diào)節(jié)機(jī)制做了大量深入的研究,目前已發(fā)現(xiàn)許多于Gq蛋白偶聯(lián)的受體激活后均能引起M電流的抑制,并且膜磷脂酰肌醇4,5二磷酸(PIP2)參與了膜受體的信號轉(zhuǎn)導(dǎo)。已證實(shí)Gq蛋白偶聯(lián)受體激活后,都會引起位于胞膜內(nèi)側(cè)的PIP2水解,產(chǎn)生IP3和DAG。已有的研究結(jié)果證實(shí)M1受體的激活引起M電流的抑制是由于PIP2的水解所為,而另外一種受體BK2受體激活后雖然也產(chǎn)生IP3和DAG,但它激活后所引起的M電流抑制是通過鈣離子介導(dǎo),由鈣調(diào)素來實(shí)現(xiàn)的。同樣是利用PLC信號通路的M1受體和BK2受體為何會分別利用PIP2和鈣離子來實(shí)現(xiàn)對M電流的調(diào)控?因此,目前對于這一問題有人提出了用微域結(jié)構(gòu)來解釋這種信號傳導(dǎo)的特異性,他們認(rèn)為BK2受體與IP3受體處于同一個微域結(jié)構(gòu)內(nèi),因此BK2受體激活后所產(chǎn)生的IP3能以較大濃度作用于附近的IP3受體,進(jìn)而引起細(xì)胞內(nèi)鈣釋放;而M受體和IP3受體卻沒有形成相應(yīng)的微域結(jié)構(gòu),因此其激活后所產(chǎn)生的IP3在局部不能形成使IP3受體激活的有效濃度,從而不能引起細(xì)胞內(nèi)鈣的釋放。上述實(shí)驗(yàn)結(jié)論是建立在以大鼠頸上交感神經(jīng)節(jié)為研究的基礎(chǔ)上而得出的。眾所周知,磷脂酶C信號通路是一種廣泛存在于眾多生命形式中的信號轉(zhuǎn)導(dǎo)機(jī)制。因此,這種信號轉(zhuǎn)導(dǎo)的差異性在其他的神經(jīng)細(xì)胞是否存在還不得而知。這一問題的闡明,將對深入了解磷脂酶C信號通路的多樣性具有至關(guān)重要的意義。 本小組前期的研究結(jié)果表明:在不同的神經(jīng)細(xì)胞中,M1,BK2,H1,AT1受體激活后雖然都可以水解PIP2,產(chǎn)生IP3和DAG,但是引發(fā)內(nèi)鈣釋放的作用之間存在明顯不同,在頸上神經(jīng)節(jié)細(xì)胞內(nèi)BK2,H1,AT1受體激活后均可以引起內(nèi)鈣的升高,而M1受體則不能。在海馬神經(jīng)細(xì)胞內(nèi),BK2,H1,M1受體激動后引起內(nèi)鈣升高,而AT1受體則不能。在HEK293細(xì)胞內(nèi),過表達(dá)M1和BK2受體引起的內(nèi)鈣釋放與神經(jīng)細(xì)胞又有所不同,二者均可以引起內(nèi)鈣升高。在爪蟾卵母細(xì)胞過表達(dá)M1和BK2受體也均可以引起內(nèi)鈣的升高。本實(shí)驗(yàn)以大鼠頸上交感神經(jīng)節(jié)細(xì)胞、海馬神經(jīng)元、HEK293細(xì)胞、爪蟾卵母細(xì)胞為研究對象,利用免疫共沉淀技術(shù)觀察不同Gq蛋白偶聯(lián)受體和位于內(nèi)質(zhì)網(wǎng)膜上IP3受體之間的關(guān)系,探究是否存在一種信號微域以及其特點(diǎn),從而為Gq蛋白偶聯(lián)受體的信號通路的多樣性尋找生化依據(jù)。 目的:利用免疫共沉淀技術(shù),在兩種不同類型的神經(jīng)細(xì)胞、HEK293細(xì)胞以及爪蟾卵母細(xì)胞,觀察不同Gq蛋白偶聯(lián)受體與內(nèi)質(zhì)網(wǎng)IP3受體之間的關(guān)系。 方法:采用免疫共沉淀(coimmunoprecipitation),SDS-PAGE,Western blot等方法觀察在頸上交感神經(jīng)節(jié)和海馬神經(jīng)元中上述四種Gq蛋白偶聯(lián)受體與內(nèi)質(zhì)網(wǎng)IP3受體之間的關(guān)系。在HEK293細(xì)胞中,利用脂質(zhì)體轉(zhuǎn)染的方法外源性表達(dá)M1、H1、AT1、BK2受體,觀察這四種受體與IP3受體的關(guān)系。在爪蟾卵母細(xì)胞中,利用體外轉(zhuǎn)錄的RNA在卵母細(xì)胞外源性表達(dá)M1和BK2受體,觀察這兩種受體與IP3受體之間的關(guān)系。 結(jié)果:⑴在頸上神經(jīng)節(jié)和海馬神經(jīng)元中,均可檢測到M1、H1、AT1、BK2受體的表達(dá)。(2)在頸上神經(jīng)節(jié)和海馬神經(jīng)元中,均可檢測到IP3受體的表達(dá)。(3)免疫共沉淀的結(jié)果表明,在頸上交感神經(jīng)節(jié)中,H1、AT1、BK2受體均可以和IP3受體共沉淀,未發(fā)現(xiàn)M1和IP3受體共沉淀。在海馬神經(jīng)元,AT1受體可以和IP3受體共沉淀,未發(fā)現(xiàn)M1、H1、BK2受體和IP3受體共沉淀。(4)在分別外源性表達(dá)M1、H1、AT1、BK2受體的HEK293細(xì)胞中,均可以分別檢測到四種受體的表達(dá)。(5)在外源性表達(dá)這四種受體的HEK293細(xì)胞中,均可以檢測到IP3受體的表達(dá)。(6)在過表達(dá)這四種受體的細(xì)胞中,M1、BK2、AT1與IP3受體共沉淀,而H1受體不能與IP3受體共沉淀。(7)在過表達(dá)M1和BK2受體的爪蟾卵母細(xì)胞中,均可以檢測到這兩種受體的過表達(dá)。(8)在過表達(dá)M1和BK2受體的爪蟾卵母細(xì)胞中,均可以檢測到IP3受體的表達(dá)。(9)在爪蟾卵母細(xì)胞中,這兩種受體均可以和IP3受體共沉淀。 結(jié)論:(1)在大鼠頸上交感神經(jīng)節(jié)細(xì)胞中中,M1受體和H1、AT1、BK2受體與IP3受體之間的關(guān)系不同,其中,H1、AT1、BK2受體與IP3受體相偶連,而M1和IP3受體之間不存在偶連關(guān)系。在海馬神經(jīng)元中,AT1和IP3受體相偶連,M1、BK2、H1受體和IP3受體之間不存在偶連關(guān)系。(2)在HEK293細(xì)胞中,M1、H1、AT1、BK2受體與IP3受體之間存在偶連關(guān)系,與神經(jīng)組織存在明顯不同。(3)在爪蟾卵母細(xì)胞中,M1和BK2受體與IP3受體之間存在偶聯(lián)關(guān)系,與HEK293細(xì)胞中的結(jié)果一致。(4)不同組織細(xì)胞中不同GPCR與IP3受體偶聯(lián)有較大差異,其細(xì)胞生理學(xué)意義有待進(jìn)一步闡明。
[Abstract]:G-protein-coupled receptors (GPCRs) are the most widely recognized class of receptors. These receptors are structurally similar, formed by a peptide chain, transmembrane seven times, N-terminus extracellular, C-terminus intracellular. These receptors and effectors are mediated by G proteins. There are many G proteins, but all types of G proteins are composed of three distinct subunits. According to the structure of the alpha subunit of G protein, it can be divided into six subfamilies: Gs, Gi/o, G q, Gt, Gg and G12 [1]. Phospholipase C (PLC) signaling system mediated by G Q protein-coupled receptors is a widespread signal transduction mechanism. First, PLC beta is activated, then the membrane PIP2 is hydrolyzed to produce two second messengers IP3 and DAG, which regulate many cellular functions, such as ion channel function, cell cycle, gland secretion, and so on.
IP3 receptor is a kind of channel protein which can induce intracellular calcium release. It can bind to IP3 and induce intracellular calcium release, which leads to the elevation of intracellular calcium level. Up to now, four IP3 receptors have been found, of which type I receptors are ubiquitous in nerve tissues. Intracellular calcium release plays an important role in cell signal transduction. In addition, abnormal calcium signaling is also involved in many pathological processes.
M current was first discovered by Brown and Admas in the superior cervical sympathetic ganglion of bullfrog in 1980. It is a slow-activated, non-inactivated voltage-dependent outward potassium current, named for its strong inhibition by muscarinic receptors. Since 1998, it has been gradually recognized that its molecular basis is the potassium channel of the KCNQ family (KCNQ2/3). Current is closely related to the excitability of the nervous system. Since the discovery of current, a great deal of research has been done on its regulation mechanism. It has been found that many Gq protein-coupled receptors can induce M-current inhibition after activation, and membrane phosphatidylinositol 4,5 diphosphate (PIP2) is involved in the letter of membrane receptors. It has been proved that the activation of Gq protein-coupled receptor can induce the hydrolysis of PIP2 and the production of IP3 and DAG on the inner surface of the cell membrane. Previous studies have shown that the inhibition of M current caused by the activation of M1 receptor is due to the hydrolysis of PIP2, while the activation of another receptor, BK2 receptor, can also produce IP3 and DAG, but the activation of the receptor causes the M current. Current inhibition is mediated by calcium ions and is achieved by calmodulin. Why do M1 receptors and BK2 receptors, which also use the PLC signaling pathway, use PIP2 and calcium ions to regulate M current respectively? Therefore, some people have proposed to explain the specificity of this signal transduction by using the micro-domain structure. They believe that BK2 receptors are affected. The body is in the same microdomain as IP3 receptor, so the IP3 produced by the activation of BK2 receptor can act on the nearby IP3 receptor at a higher concentration, and then induce intracellular calcium release; while the M receptor and IP3 receptor do not form the corresponding microdomain structure, so the IP3 produced by the activation of BK2 receptor can not form the IP3 receptor activated locally. These results are based on the study of the rat superior cervical sympathetic ganglion. It is well known that the phospholipase C signaling pathway is a signal transduction mechanism that exists widely in many forms of life. Therefore, the differences in this signal transduction are among other gods. It is not known whether the cells exist or not. The clarification of this question will be of great significance to the further understanding of the diversity of phospholipase C signaling pathways.
Previous studies by our team have shown that in different nerve cells, M1, BK2, H1, AT1 receptors can hydrolyze PIP2 and produce IP3 and DAG after activation, but there are significant differences in the role of intracellular calcium release. In the superior cervical ganglion cells, BK2, H1, AT1 receptors can activate the increase of intracellular calcium, while M1 receptors can not. In hippocampal neurons, the activation of BK2, H1 and M1 receptors results in elevation of intracellular calcium, whereas AT1 receptors do not. In HEK293 cells, the release of intracellular calcium caused by overexpression of M1 and BK2 receptors is different from that of neurons, both of which can cause elevation of intracellular calcium. Overexpression of M1 and BK2 receptors in Xenopus oocytes can also cause elevation of intracellular calcium. The relationship between different Gq protein-coupled receptors and IP3 receptors located on the endoplasmic reticulum was observed by immunoprecipitation technique in rat superior cervical sympathetic ganglion cells, hippocampal neurons, HEK293 cells and Xenopus oocytes, and whether there was a signal microdomain and its characteristics were explored in order to provide Gq protein-coupled receptors. The diversity of signal pathways is to find biochemical evidence.
AIM: To investigate the relationship between different Gq protein-coupled receptors and endoplasmic reticulum IP3 receptors in two different types of nerve cells, HEK293 cells and Xenopus oocytes by immunoprecipitation technique.
Methods: The relationship between these four Gq protein-coupled receptors and endoplasmic reticulum IP3 receptors in superior cervical sympathetic ganglion and hippocampal neurons was observed by immunoprecipitation, SDS-PAGE and Western blot. In Xenopus oocytes, M1 and BK2 receptors were exogenously expressed in Xenopus oocytes using in vitro transcripted RNA. The relationship between these two receptors and IP3 receptors was observed.
Results: (1) The expression of M1, H1, AT1 and BK2 receptors was detected in both superior cervical ganglion and hippocampal neurons. (2) The expression of IP3 receptors was detected in both superior cervical ganglion and hippocampal neurons. (3) The results of immunoprecipitation showed that H1, AT1, BK2 receptors could co-precipitate with IP3 receptors in superior cervical sympathetic ganglion, but no M1 and IP3 receptors were found. Receptor coprecipitation. In hippocampal neurons, AT1 receptor can coprecipitate with IP3 receptor, but no coprecipitation of M1, H1, BK2 receptor and IP3 receptor was found. (4) In HEK293 cells expressing exogenous M1, H1, AT1 and BK2 receptors respectively, the expression of four receptors can be detected. (5) In HEK293 cells expressing these four receptors, the expression of these receptors can be detected. To the expression of IP3 receptors. (6) M1, BK2, AT1 and IP3 receptors co-precipitated in cells overexpressing these four receptors, while H1 receptors could not co-precipitate with IP3 receptors. (7) Overexpression of these two receptors was detected in Xenopus oocytes overexpressing M1 and BK2 receptors. (8) Both M1 and BK2 receptors could be detected in Xenopus oocytes overexpressing Xenopus oocytes. The expression of IP3 receptor was detected. (9) In Xenopus oocytes, both receptors could coprecipitate with IP3 receptor.
CONCLUSIONS: (1) The relationship between M1 receptor, H1, AT1, BK2 receptor and IP3 receptor is different in rat superior cervical sympathetic ganglion cells. H1, AT1, BK2 receptor and IP3 receptor are coupled, but there is no coupling between M1 and IP3 receptor. In hippocampal neurons, there is no coupling between AT1 and IP3 receptor, M1, BK2, H1 receptor and IP3 receptor. (2) In HEK293 cells, M1, H1, AT1, BK2 receptors were associated with IP3 receptors, which were significantly different from nerve tissues. (3) In Xenopus oocytes, there was a coupling relationship between M1 and BK2 receptors and IP3 receptors, which was consistent with the results of HEK293 cells. (4) GPCR and IP3 receptors were coupled differently in different tissues and cells. Its cellular physiological significance needs to be further elucidated.
【學(xué)位授予單位】：河北醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2007
【分類號】：R33

【相似文獻(xiàn)】

相關(guān)期刊論文 前10條

1 楊亮;楊細(xì)飛;張毅;劉建軍;李杰;;利用免疫共沉淀技術(shù)驗(yàn)證SET與eEF1A1在人肝細(xì)胞內(nèi)的相互作用[J];安徽農(nóng)業(yè)科學(xué);2010年35期

2 劉一平,鄧?yán)^先,張英麗,呂婭歆,程萱,黃翠芬;用免疫共沉淀進(jìn)一步確定SMAD4中間連接區(qū)在形成同源和異源復(fù)合物時的作用[J];中國生物化學(xué)與分子生物學(xué)報(bào);2000年04期

3 孫玉靜,楊守京,劉彥仿;漢坦病毒感染乳鼠腦組織中HSP70與病毒抗原關(guān)系[J];臨床與實(shí)驗(yàn)病理學(xué)雜志;2002年05期

4 高娟,楊守京,劉彥仿;漢灘病毒結(jié)構(gòu)蛋白與該病毒感染誘導(dǎo)表達(dá)的多種熱休克蛋白的研究[J];中華傳染病雜志;2004年05期

5 高婧;董長垣;胡俊;李艷;Joseph K K Li;戴瑩;郭淑芳;;HBV X蛋白與宿主APOBEC3G蛋白之間的相互作用[J];武漢大學(xué)學(xué)報(bào)(理學(xué)版);2007年04期

6 王春美;盛光耀;盧潔;鄒湘;方營旗;白松婷;謝壘;;免疫共沉淀檢測人p65和SMRT蛋白間相互作用[J];山東大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2010年10期

7 胡小曉,熊熙文,周建林,張健;小鼠腫瘤致死因子α誘導(dǎo)的TNFAIP1蛋白與DNA聚合酶δ亞單位的相互作用[J];湖南師范大學(xué)自然科學(xué)學(xué)報(bào);2004年03期

8 王震;劉冬青;王茵;屈伸;孟憲敏;;Nelin與F-actin及Filamin相互作用的鑒定[J];華中科技大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2007年03期

9 張方;施毅;辛?xí)苑?劉玉秀;錢桂生;羅向東;宋勇;李子玲;;大鼠肺泡巨噬細(xì)胞Bcl-2相關(guān)抗凋亡蛋白-1表達(dá)變化及其調(diào)節(jié)糖皮質(zhì)激素受體功能的研究[J];醫(yī)學(xué)研究生學(xué)報(bào);2007年11期

10 王鴻杰;張志文;;用酵母雙雜交系統(tǒng)篩選ATF5相互作用蛋白[J];中國生物化學(xué)與分子生物學(xué)報(bào);2008年02期

相關(guān)會議論文 前10條

1 邱峰;毛小琴;陳世知;邱宗蔭;;GBLP相互作用蛋白研究[A];2008年中國藥學(xué)會學(xué)術(shù)年會暨第八屆中國藥師周論文集[C];2008年

2 邵偉;劉成國;;幽門螺桿菌CagA蛋白干擾細(xì)胞信息通路能力獨(dú)立于不同胃疾狀態(tài)[A];2008年浙江省內(nèi)科學(xué)學(xué)術(shù)會議論文匯編[C];2008年

3 龍鼎新;伍一軍;;神經(jīng)病靶酯酶的泛素化降解及ARA54的調(diào)節(jié)[A];湖南省生理科學(xué)會2008年度學(xué)術(shù)年會論文摘要匯編[C];2008年

4 池志強(qiáng);;G蛋白偶聯(lián)受體二聚體研究進(jìn)展[A];第八屆全國生化藥理學(xué)術(shù)討論會暨第七屆Servier獎頒獎大會會議摘要集[C];2003年

5 彭旭;譚江琳;袁順宗;馬兵;賀偉峰;黃正根;程文廣;賈雄飛;王曉娟;胡婕;甘成軍;陳希煒;胡曉紅;張小容;羅高興;吳軍;;免疫共沉淀技術(shù)驗(yàn)證HT036與P311間的相互作用[A];中華醫(yī)學(xué)會燒傷外科學(xué)分會2009年學(xué)術(shù)年會論文匯編[C];2009年

6 張照環(huán);徐曉輝;張勇;周建峰;俞仲望;何成;;LINGO-1與WNK1結(jié)合并調(diào)節(jié)Nogo誘導(dǎo)的軸突延長抑制[A];中華醫(yī)學(xué)會第十三次全國神經(jīng)病學(xué)學(xué)術(shù)會議論文匯編[C];2010年

7 梁淑芳;于延豹;許雪嬌;宋培明;薛燕;楊們原;陳先;;基于氨基酸同位素代謝標(biāo)記的免疫共沉淀分析蛋白質(zhì)相互作用[A];中國蛋白質(zhì)組學(xué)第三屆學(xué)術(shù)大會論文摘要[C];2005年

8 李占潮;周漩;戴宗;鄒小勇;;基于支持向量機(jī)預(yù)測G蛋白偶聯(lián)功能類[A];第十屆全國計(jì)算(機(jī))化學(xué)學(xué)術(shù)會議論文摘要集[C];2009年

9 王震;孟憲敏;郭蓮軍;;人類新基因Nelin及其生物學(xué)特性的研究[A];湖北省暨武漢生物化學(xué)與分子生物學(xué)學(xué)會第八屆會員代表大會和第十五次學(xué)術(shù)年會論文摘要匯編[C];2004年

10 孟鳳艷;何夏萍;王亞軍;蔣小松;李娟;;家雞似降鈣素受體基因的克隆、序列分析以及組織表達(dá)圖譜探究[A];中國動物遺傳育種研究進(jìn)展——第十五次全國動物遺傳育種學(xué)術(shù)討論會論文集[C];2009年

相關(guān)重要報(bào)紙文章 前9條

1 ;重視微循環(huán)研究 為臨床應(yīng)用服務(wù)[N];中國醫(yī)藥報(bào);2003年

2 陳衛(wèi)東;我發(fā)現(xiàn)交感神經(jīng)系統(tǒng)調(diào)控免疫“鑰匙”[N];科技日報(bào);2004年

3 汪敏華;細(xì)胞信號轉(zhuǎn)導(dǎo)之謎解開[N];解放日報(bào);2004年

4 陸志城;黑色素濃縮激素與多種現(xiàn)代病有關(guān)[N];醫(yī)藥經(jīng)濟(jì)報(bào);2002年

5 張中橋;猴病毒40——腦腫瘤發(fā)生的“罪魁”[N];中國醫(yī)藥報(bào);2001年

6 張中橋;猴病毒40與腦腫瘤發(fā)生有相關(guān)性[N];醫(yī)藥經(jīng)濟(jì)報(bào);2001年

7 記者 陸葉清;發(fā)現(xiàn)抑制胃癌細(xì)胞的重要基因[N];上海科技報(bào);2010年

8 記者 孫國根;人類分娩啟動機(jī)制研究獲進(jìn)展[N];健康報(bào);2011年

9 張艷敏　唐發(fā)發(fā) 孫雨;扎根國土 引領(lǐng)國際甲胎蛋白研究[N];科技日報(bào);2011年

相關(guān)博士學(xué)位論文 前10條

1 龔先瓊;乙型肝炎病毒表面抗原與烯酰輔酶A水合酶相互作用及對細(xì)胞凋亡的影響[D];福建醫(yī)科大學(xué);2012年

2 蘭世杰;BCCIP相互作用蛋白的鑒定與功能研究[D];吉林大學(xué);2012年

3 周偉強(qiáng);DOC-1R基因?qū)?xì)胞增殖周期影響的研究[D];中國醫(yī)科大學(xué);2003年

4 許放;G蛋白偶聯(lián)受體介導(dǎo)雄激素對前列腺癌細(xì)胞快速作用的非基因組機(jī)制[D];第二軍醫(yī)大學(xué);2006年

5 倪燕翔;G蛋白偶聯(lián)受體調(diào)節(jié)β淀粉樣蛋白的產(chǎn)生[D];中國科學(xué)院研究生院（上海生命科學(xué)研究院）;2005年

6 孫濤;腫瘤細(xì)胞成血管塑形在血管生成擬態(tài)形成中的作用研究[D];天津醫(yī)科大學(xué);2010年

7 束峰玨;人類絲氨酸/蘇氨酸激酶Aik與細(xì)胞周期調(diào)控的關(guān)系探討[D];復(fù)旦大學(xué);2002年

8 高霄飛;表皮生長因子對背根神經(jīng)節(jié)神經(jīng)元內(nèi)向整流型鉀離子通道調(diào)節(jié)的研究[D];第二軍醫(yī)大學(xué);2005年

9 李中秋;Neuroglobin在視網(wǎng)膜中的表達(dá)及其保護(hù)視網(wǎng)膜缺血缺氧損傷分子機(jī)制的研究[D];吉林大學(xué);2006年

10 黃增榮;幽門螺桿菌空泡毒素與線粒體腺嘌呤核苷酸轉(zhuǎn)移酶相互作用的研究[D];西北農(nóng)林科技大學(xué);2010年

相關(guān)碩士學(xué)位論文 前10條

1 梁惠玲;多種細(xì)胞體系G_q蛋白偶聯(lián)受體和IP3受體偶聯(lián)的研究[D];河北醫(yī)科大學(xué);2007年

2 陳卿;免疫共沉淀蛋白芯片分析方法及其應(yīng)用的研究[D];中國人民解放軍軍事醫(yī)學(xué)科學(xué)院;2010年

3 孫婷婷;免疫共沉淀聯(lián)合質(zhì)譜篩選肝核因子HNF3β相互作用蛋白質(zhì)及初步功能研究[D];安徽醫(yī)科大學(xué);2011年

4 張靜;自然臨產(chǎn)前后與NF-κB相互作用蛋白質(zhì)的研究[D];中南大學(xué);2012年

5 楊陽;智力低下相關(guān)蛋白FXR1P與FTH1及CMAS相互作用的研究[D];南華大學(xué);2010年

6 劉巧姝;在自然臨產(chǎn)和藥物臨產(chǎn)中與NF-κB相互作用的蛋白質(zhì)的研究[D];中南大學(xué);2012年

7 李成華;KChIP1在KV4.3膜運(yùn)輸中的作用[D];中南大學(xué);2003年

8 張文婷;LOH12CR1互作蛋白DAPK3的鑒定[D];中南大學(xué);2012年

9 黎亮;RANBP9在早幼粒細(xì)胞白血病發(fā)生中的作用研究[D];重慶醫(yī)科大學(xué);2012年

10 伍志強(qiáng);LRP16調(diào)控NF-κB信號通路的研究[D];中國人民解放軍軍醫(yī)進(jìn)修學(xué)院;2011年

，

本文編號：2251206