排序方式: 共有38条查询结果,搜索用时 718 毫秒
11.
H. Riezman A. Munn M. I. Geli L. Hicke 《Cellular and molecular life sciences : CMLS》1996,52(12):1033-1041
Endocytosis is a general term that is used to describe the internalization of external and plasma membrane molecules into the cell interior. In fact, several different mechanisms exist for the internalization step of this process. In this review we emphasize the work on the actin-dependent pathways, in particular in the yeastSaccharomyces cerevisiae, because several components of the molecular machinery are identified. In this yeast, the analysis of endocytosis in various mutants reveals a requirement for actin, calmodulin, a type I myosin, as well as a number of other proteins that affect actin dynamics. Some of these proteins have homology to proteins in animal cells that are believed to be involved in endocytosis. In addition, the demonstration that ubiquitination of some cell surface molecules is required for their efficient internalization is described. We compare the actin, myosin and ubiquitin requirements for endocytosis with recent results found studying these processes usingDictyostelium discoideum and animal cells. 相似文献
12.
Incorporation of E-cadherin into the adherens junction is a highly regulated process required to establish
firm cell-cell adhesion in most epithelia. Less is known about the mechanisms that govern the clearance of
E-cadherin from the cell surface in both normal and pathological states. In this study, we found that the
steady-state removal of E-cadherin in primary cultured pig thyroid cell monolayers is slow and involves
intracellular degradation. Experimental abrogation of adhesion by a Ca2+ switch induces
rapid cell surface proteolysis of E-cadherin. At the same time, endocytosed intact E-cadherin and newly
synthesized E-cadherin accumulate in intracellular compartments that largely escape further degradation. Acute
stimulation with thyroid-stimulating hormone (TSH) or forskolin prevents all signs of accelerated E-cadherin
turnover. The findings indicate that TSH receptor signaling via cyclic AMP stabilizes the assembly and retention
of E-cadherin at the cell surface. This suggests a new mechanism by which TSH supports maintenance of thyroid
follicular integrity.Received 23 February 2004; received after revision 14 May 2004; accepted 26 May 2004 相似文献
13.
Alvi F Idkowiak-Baldys J Baldys A Raymond JR Hannun YA 《Cellular and molecular life sciences : CMLS》2007,64(3):263-270
The protein kinase C (PKC) family of isoenzymes has been shown to regulate a variety of cellular processes, including receptor
desensitization and internalization, and this has sparked interest in further delineation of the roles of specific isoforms
of PKC in membrane trafficking and endocytosis. Recent studies have identified a novel translocation of PKC to a juxtanuclear
compartment, the pericentrion, which is distinct from the Golgi complex but epicentered on the centrosome. Sustained activation
of PKC (longer than 30 min) also results in sequestration of plasma membrane lipids and proteins to the same compartment,
demonstrating a global effect on endocytic trafficking. This review summarizes these studies, particularly focusing on the
characterization of the pericentrion as a distinct PKC-dependent subset of recycling endosomes. We also discuss emerging insights
into a role for PKC as a central hub in regulating vesicular transport pathways throughout the cell, with implications for
a wide range of pathobiologic processes, e.g. diabetes and abnormal neurotransmission or receptor desensitization.
Received 11 August 2006; received after revision 20 September 2006; accepted 7 November 2006 相似文献
14.
Delivery of macromolecules into living cells by arginine-rich cell penetrating peptides (AR-CPPs) is an important new avenue
for the development of novel therapeutic strategies. However, to date the mechanism of this delivery remains elusive. Recent
data implicate endocytosis in the internalization of AR-CPPs and their macromolecular cargo and also indicate limited delivery
of macromolecules into the cell cytoplasm and nucleus. Different types of endocytosis – clathrin-dependent endocytosis, raft/caveolin-dependent
endocytosis and macropinocytosis – are all implicated in the uptake of AR-CPPs and their cargo into different cells. Cationic
AR-CPPs dramatically increase uptake of conjugated molecules through efficient binding to surface proteoglycans. Whether this
increase in binding can assure delivery of a sufficient amount of functionally active macromolecules into the cytoplasm and
nucleus or whether there is a specific mechanism by which AR-CPPs facilitate the escape of conjugated cargo from endosomes
remains to be understood.
Received 30 June 2005; received after revision 9 August 2005; accepted 30 August 2005 相似文献
15.
Jacquet S Malaval C Martinez LO Sak K Rolland C Perez C Nauze M Champagne E Tercé F Gachet C Perret B Collet X Boeynaems JM Barbaras R 《Cellular and molecular life sciences : CMLS》2005,62(21):2508-2515
Cell surface receptors for high-density lipoprotein (HDL) on hepatocytes are major partners in the regulation of cholesterol
homeostasis. We recently identified a cell surface ATP synthase as a high-affinity receptor for HDL apolipoprotein A-I (apoA-I)
on human hepatocytes. Stimulation of this ectopic ATP synthase by apoA-I triggered a low-affinity-receptor-dependent HDL endocytosis
by a mechanism strictly related to the generation of ADP. This suggests that nucleotide G-protein- coupled receptors of the
P2Y family are molecular components in this pathway. Only P2Y1 and P2Y13 are present on the membrane of hepatocytes. Using both a pharmacological approach and small interference RNA, we identified
P2Y13 as the main partner in hepatic HDL endocytosis, in cultured cells as well as in situ in perfused mouse livers. We also found
a new important action of the antithrombotic agent AR-C69931MX as a strong activator of P2Y13-mediated HDL endocytosis.
Received 9 May 2005; received after revision 24 June 2005; accepted 1 September 2005 相似文献
16.
Genetic and molecular analysis of the synaptotagmin family 总被引:5,自引:0,他引:5
Secretion is a fundamental cellular process used by all eukaryotes to insert proteins into the plasma membrane and transport
signaling molecules and intravesicular proteins into the extracellular space. Secretion requires the fusion of two phospholipid
bilayers within the cell, an energetically unfavorable process. A conserved repertoire of vesicle-trafficking proteins has
evolved that function to overcome this energy barrier and temporally and spatially control membrane fusion within the cell.
Within neurons, opening of synaptic calcium channels and subsequent calcium entry triggers synchronous synaptic vesicle exocytosis
and neurotransmitter release into the synaptic cleft. After fusion, synaptic vesicles undergo endocytosis, are refilled with
neurotransmitter, and return to the vesicle pool for further rounds of cycling. It is within this local synaptic trafficking
pathway that the synaptotagmin family of calcium-binding synaptic vesicle proteins has been postulated to function. Here we
review the current literature on the function of the synaptotagmin family and discuss the implications for synaptic transmission
and membrane trafficking.
Received 14 August 2000; received after revision 20 September 2000, accepted 14 October 2000 相似文献
17.
主要观察了外源生长素长时间(8 h)处理对拟南芥生长素极性输出载体PIN2-GFP质膜丰度的影响,低温、KCN处理和生长素受体突变对生长素调控质膜PIN2-GFP丰度的影响,以及液泡H+-ATPase抑制剂ConA对野生型和生长素受体四突变体tir1afb1,2,3液泡中PIN2-GFP积累的影响.结果表明:外源生长素通过其受体TIR1/AFB介导的信号途径下调质膜PIN2-GFP的丰度,促进PIN2-GFP的内吞、胞内运输和液泡降解.暗示生长素通过TIR1/AFB介导的信号途径反馈调控质膜PIN2-GFP的水平,从而阻止了胞内生长素的过多输出. 相似文献
18.
时文东 《清华大学学报(自然科学版)》2009,(2)
为研究纳米颗粒进入具有自发曲率的细胞膜的机理,在已建立的受体介导胞吞作用力学模型的基础上进行了扩展,对非零自发曲率的细胞膜上发生的受体介导的胞吞作用进行了研究。结果显示:包裹时间不仅依赖于颗粒的尺寸,而且依赖于细胞膜的自发曲率;存在最佳的颗粒半径使包裹时间最短;对于无限大尺寸的细胞膜,当细胞膜的自发曲率大于临界值时,存在最小和最大包裹半径,但当细胞膜的自发曲率小于等于临界值时,只存在最小包裹半径。 相似文献
19.
主要阐述了网格蛋白、接头蛋白AP2复合体的组成及其功能、动物网格蛋白介导内吞的分子机制和植物网格蛋白介导内吞的一些最新进展;阐述了植物网格蛋白介导的内吞在生长素极性运输、胚胎发育及逆境响应等中的作用,总结了植物网格蛋白介导内吞的生物学意义及展望. 相似文献
20.
Huntington’s disease (HD) is caused by a polyglutamine expansion in the protein huntingtin and is characterized by intraneuronal inclusions and widespread neuronal death at the late stage of the disease. In research, most of the emphasis has been on understanding the cell death and its mechanisms. Until recently, it was believed that the vast majority, if not all, of the symptoms in HD are a direct consequence of neurodegeneration. However, increasing evidence shows that subtle alterations in synaptic function could underlie the early symptoms. It is of particular interest to understand the nature of this neuronal dysfunction. Normal huntingtin interacts with various cytoskeletal and synaptic vesicle proteins that are essential for exocytosis and endocytosis. Altered interactions of mutant huntingtin with its associated partners could contribute to abnormal synaptic transmission in HD. This review describes recent advances in understanding synaptic dysfunction in HD.Received 2 March 2005; received after revision 13 April 2005; accepted 19 April 2005 相似文献