信號轉(zhuǎn)導(dǎo)手冊

內(nèi)容概要

Ralph
A.Bradshaw編著的《信號轉(zhuǎn)導(dǎo)手冊(1細胞內(nèi)外信號轉(zhuǎn)導(dǎo)機制原著第2版導(dǎo)讀版)(精)》包含350個章節(jié)，全面涵蓋細胞信號轉(zhuǎn)導(dǎo)領(lǐng)域。內(nèi)容包括：細胞內(nèi)外信號轉(zhuǎn)導(dǎo)機制，蛋白質(zhì)磷酸化和去磷酸化，鈣離子信號轉(zhuǎn)導(dǎo)、脂質(zhì)介導(dǎo)的第二信使，蛋白質(zhì)互作、環(huán)化核苷酸，G蛋白、發(fā)育生物學(xué)中的信號轉(zhuǎn)導(dǎo)，轉(zhuǎn)錄與翻譯：細胞核與細胞質(zhì)事件．細胞內(nèi)功能區(qū)隔信號轉(zhuǎn)導(dǎo)、胞間和細胞基質(zhì)問的相互作用、疾病病理學(xué)。
《信號轉(zhuǎn)導(dǎo)手冊(1細胞內(nèi)外信號轉(zhuǎn)導(dǎo)機制原著第2版導(dǎo)讀版)(精)》是生物學(xué)實驗室不可或缺的工具用書，適用于生物化學(xué)與分子生物學(xué)、細胞生物學(xué)等相關(guān)專業(yè)的高年級本科生、研究生．也可作為教師的教學(xué)和科研參考書，亦可供生物醫(yī)學(xué)、藥理學(xué)、免疫學(xué)及相關(guān)領(lǐng)域的研究人員參考。

書籍目錄

英文目錄
撰稿人名單
第二版前言
第一版前言
導(dǎo)讀版第①卷  細胞內(nèi)外信號轉(zhuǎn)導(dǎo)機制
    l．細胞信號轉(zhuǎn)導(dǎo)：昨天、今天和明天
第一部分  起始：胞外及質(zhì)膜事件
  A  分子識別
    2．分子識別的結(jié)構(gòu)和能量基礎(chǔ)
    3．蛋白與蛋白相互作用的自由能概貌
    4．分子社會學(xué)
    5．抗原一抗體識別及其構(gòu)象變化
    6．抗原一抗體界面處的結(jié)合熱力學(xué)
    7．免疫球蛋白-Fc受體相互作用
    8．免疫球蛋白超折疊及其在分子識別中的多種用途
    9．T細胞受體／pMHc復(fù)合體
    10．細胞表面黏附受體的機制特征
    11．免疫突觸
    12．NK受體
    13．碳水化合物的識別與信號轉(zhuǎn)導(dǎo)
    14．鼻病毒與其受體的相互作用
    15．卜型人免疫缺陷病毒與其受體的相互作用
    16．流感病毒神經(jīng)氨酸酶的抑制劑
    17．涉及血液纖維蛋白原及纖維蛋白的信號事件的結(jié)構(gòu)基礎(chǔ)
    18．整合素信號的結(jié)構(gòu)基礎(chǔ)
    19．G蛋白異源三聚體及其復(fù)合物的結(jié)構(gòu)
    20．G蛋白偶聯(lián)受體的結(jié)構(gòu)
    21．Toll樣受體的結(jié)構(gòu)與信號
    22．多種多樣的淋巴細胞受體
  B  多通路受體
    23．G蛋白偶聯(lián)受體的結(jié)構(gòu)與功能：從最近發(fā)現(xiàn)的晶體結(jié)構(gòu)得到的啟示
    24．趨化因子及其受體的結(jié)構(gòu)與功能
    25．G蛋白偶聯(lián)受體的結(jié)構(gòu)及其被可擴散激素所激活的過程(參照β2型腎上腺素受體模型)
    26．蛋白酶激活的受體
    27．由激動劑導(dǎo)致的G蛋白偶聯(lián)受體的脫敏及細胞內(nèi)吞化作用
    28．由G蛋白偶聯(lián)受體形成的二聚化復(fù)合體的功能
    29．細菌中的趨化性受體：跨膜信號，敏感性，匹配及受體聚集
    30．離子通道結(jié)構(gòu)概論
    31．STIM和Orai介導(dǎo)的鈣庫依賴性鈣信號及CRAC離子通道激活的分子機制
    32．離子滲入性：離子選擇性與進入阻斷的機制
    33．煙堿乙酰膽堿受體
    34．與核苷酸環(huán)化酶直接結(jié)合而被調(diào)節(jié)的離子通道
  C  對受體的橫向比較研究
    35．細胞因子受體概述
    36．生長激素與泌乳激素家族及其受體：受體激活和調(diào)節(jié)的結(jié)構(gòu)基礎(chǔ)
    37．以促紅細胞生成素受體為例的細胞因子信號
    38．纖維原細胞生長因子(FGF)信號復(fù)合體
    39．γ干擾素及其受體的結(jié)構(gòu)
導(dǎo)讀版第2卷  蛋白質(zhì)磷酸化和去磷酸化
導(dǎo)讀版第3卷  鈣離子信號轉(zhuǎn)導(dǎo)、脂質(zhì)介導(dǎo)的第二信使
導(dǎo)讀版第4卷  蛋白質(zhì)互作、環(huán)化核苷酸
導(dǎo)讀版第5卷  G蛋白、發(fā)育生物學(xué)中的信號轉(zhuǎn)導(dǎo)
導(dǎo)讀版第6卷  轉(zhuǎn)錄與翻譯：細胞核與細胞質(zhì)事件
導(dǎo)讀版第7卷  細胞內(nèi)功能區(qū)隔信號轉(zhuǎn)導(dǎo)、胞間和細胞基質(zhì)間的相互作用、疾病病理學(xué)
索引

章節(jié)摘錄

　　Mechanistic Features of Cell-Surface Adhesion Receptors　　Living cells constantly interact with their environment.Asa consequence，a number of sensory systems have evolvedfor the collection，processing，and integration ot a remark-able range of environmental stimuli arising from cell-celland cell-substrate interactions.For instance，developmentaland morphological processes in higher eukaryotes rely onthe orchestrated migration of cells in response to specificphysical and chemical cues；T cell activation relies on thelocalization and comDartmentalization of cell-adhesion andsignaling molecules；and adherent cells must respond to avariety of intracellular and extracellular mechanical forces.All of these processes rely on the engagement ot spemhc cell-surface receptors with the appropriate extracellularligand to report on the immediate physical environment bytransducing extracellular signals across the plasma mem-brane.This review examines the diversity of mechanismsthought to be involved in adhesion and signaling and high-1ights some of the shared principles that must be consideredfor all signaling pathways utilizing cell-surface receptors.　　MECHANOSENSORY MECHAN ISMS　　The ability to detect and respond to alterations in applied mechanical force is required for a number of cellular and developmental functions.This is particularly critical for adherent cells that directly contact the extracellular matrixfECM）and are subject to considerable physical deforma-tion.For example，sheer forces associated with blood flow are maior determinants of arterial tone and vascular reorgan-ization.At the cellular level，morphology and orientation are optimized to minimize mechanical stress and damage asso-ciated with variations in flow-related forces（see，for exam-ple，（1-31）.Similarly,fibroblasts must be highly responsive Handbook of Cell Signaling，Three-Volume Set 2 ed-Copyright 0 2010 Elsevier Inc All rights reservedto the mechanical forces associated with alterations in theECM（reviewed in 141）.　　Considerable evidence points to focal adhesions，thesites of cell-substrate contact，as the sensors of mechanicalforce.Central to focal adhesion assembly and function arethe integrins.a family of α-βheterodimeric transmembraneglycoproteins that provide essential adhesive functions forcell migration and the establishment and maintenance of nor-mal tissue architecture.At least 18α and 8β chains allow forthe formation of multiple integrin heterodimers that are ableto display a spectrum of specificities for cell-surface adhesion molecules and for a range of ECM components，includingLaminin，collagen，and fibronectin.The integrin cytoplas-mic domains bind a variety of scaffolding and actin regula-tory proteins.which in tum recruit a large number of adaptor and signaling molecules.These physical links couple theintegrins to the downstream activation of numerous sxgnal-ing molecules，including MAP kinase，focal adhesion kinase，Src.and P13-kinase（see，for example，（4，51）.Furthermore，integrin affinity is modulated by the activation state of the particular cell in question.

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