Titlebook: Receptor Regulation; R. J. Lefkowitz (Professor of Medicine) Book 1981 Springer Science+Business Media Dordrecht 1981 biology.cell.cell bi

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書目名稱Receptor Regulation影響因子(影響力)




書目名稱Receptor Regulation影響因子(影響力)學(xué)科排名




書目名稱Receptor Regulation網(wǎng)絡(luò)公開度




書目名稱Receptor Regulation網(wǎng)絡(luò)公開度學(xué)科排名




書目名稱Receptor Regulation被引頻次




書目名稱Receptor Regulation被引頻次學(xué)科排名




書目名稱Receptor Regulation年度引用




書目名稱Receptor Regulation年度引用學(xué)科排名




書目名稱Receptor Regulation讀者反饋




書目名稱Receptor Regulation讀者反饋學(xué)科排名

GRACE

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EGF: Receptor Interactions and the Stimulation of Cell Growth,nter, 1978), this manuscript will attempt to focus primarily on the interactions of EGF with membrane receptors. This has been for the past five years a rapidly evolving area of investigation by a number of groups. Although many gross facets of receptor control have been explored, little is actually

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Regulation of Prolactin Receptors in Target Cells,s important in regulating the functions of many organs in many species. In the mammals, the mammary gland is undoubtedly one of the principal target organs of prolactin. In this tissue, prolactin is a lactogenic and a mitogenic hormone (Cowie and Tindal, 1971; Ceriani, 1974). The biological actions

Enteropathic

Regulation of Adrenergic Receptors,ntinues to invoke investigative effort after many years of research. It has become apparent that both the release and biological actions of these mediators are modulated very specifically by pharmacological and pathological states. An understanding of the mechanisms of modulation of adrenergic actio

interpose

Denervation: Cholinergic Receptors of Skeletal Muscle, denervation supersensitivity in any denervated tissue is considered in keeping with Cannon’s ‘Law’ (see Cannon and Rosenblueth, 1949). With no . reason to expect it, physiologists have found that denervated tissues responded to the appropriate neurotransmitter with heightened sensitivity. Do the sa

CEDE

單調(diào)女

Myasthenia Gravis and the Nicotinic Cholinergic Receptor,her the cause of this autoimmune response, nor a specific treatment for curing MG is known. However, a great deal has been learned about the pathological mechanisms by which the autoimmune response to AChR impairs neuromuscular transmission, thereby causing muscular weakness. Much of our understandi

Rejuvenate

EGF: Receptor Interactions and the Stimulation of Cell Growth, known with certainty about the finer biochemical details. Within the limitations of this framework, we will attempt to integrate and evaluate present thinking concerning EGF:receptor interactions, focusing primarily on the work from the authors’ laboratories.