What is Fast Endophilin-Mediated Endocytosis?

FEME is a novel clathrin-independent endocytic pathway, regulated by the BAR domain protein endophilin, where tubulo-vesicular carriers form within seconds at the plasma membrane upon activation of specific G-protein coupled receptors (GPCRs) by their ligands, internalizing GPCRs and moving rapidly towards the perinucleolar area. Read more..

How does exocytosis affect cell mechanics?

The recycling and delivery of membrane by exocytosis can be used by the cell to enlarge the membrane and surface area during cell shape changes.The interaction between membrane tension, unfolding and trafficking has been demonstrated by a number of studies. Read more..

Exocytosis is defined as the transport and fusion of secretory vesicles with the plasma membrane and the extracellular space. There are three exocytosis pathways that deliver vesicles to the plasma membrane. Read more..

How do clathrin-coated vesicles invaginate and mature?

Clathrin-coated vesicle maturation incorporates the activities of a range of proteins. Actin, myosin and WASP all have important roles in the formation and stabilization of clathrin-coated pits (CCPs). Read more..

What causes the narrowing of clathrin-coated vesicle necks?

In the final stages of clathrin-coated vesicle (CCV) formation, Phosphatidylinositol-4,5-bisphosphate (PIP2) undergoes a dephosphorylation by phosphatases such as synaptojanin 1 (Synj1). This promotes further membrane curvature at the vesicle bud, dissociation of the BAR domain proteins (BDPs) and closing of the membrane bud neck. Read more..

How do clathrin-coated pits form?

Adaptor proteins such as AP-2, AP180 and CALM (Clathrin-assembly lymphoid myeloid leukaemia protein), which accumulate within the lipid bilayer, are responsible for the recruitment of the triskelion shaped Clathrin trimer. This trimer does not interact with the membrane directly but instead forms a reinforcing lattice structure that acts as a mold in which membrane vesicles may develop. Read more..

How does dynamin help in the scission of clathrin-coated vesicles?

In mammalian CME the GTPase dynamin is believed to play important roles in invagination and clathrin-coated pit (CCP) maturation. Its binding partners endophilin and amphiphysin, can also induce tubulation of the vesicles and have been shown to copolymerize with dynamin. Read more..

How are clathrin-coated vesicles uncoated?

Uncoating is the process by which clathrin is removed from clathrin-coated vesicles (CCVs). In mammals, this ATP dependent process is driven by the 70kDa molecular chaperone ‘Heat shock cognate protein’. Read more..

How are clathrin-coated vesicles targeted to endosomes for fusion?

Different cytoskeletal networks have been implicated in the transport of clathrin-coated vesicles (CCVs). In yeast, the actin cytoskeleton traffics dissociated CCVs, whilst in mammals the microtubule network transports is involved in the sorting of CCVs to distinct populations of early endosomes. Read more..

What is clathrin-mediated endocytosis?

Clathrin-mediated endocytosis (CME) is a vesicular transport event that facilitates the internalization and recycling of receptors engaged in a variety of processes, including signal transduction (G-protein and tyrosine kinase receptors), nutrient uptake and synaptic vesicle reformation. Two classical examples of CME are iron-bound transferrin recycling and the uptake of low-density lipoprotein (LDL). Read more..

How is caveolar endocytosis mechanically regulated?

The cell cytoskeleton plays a role in caveolar organization and trafficking. Actin stress fibers influence the linear distribution of caveolae at the plasma membrane in many cell types. Read more..

What is caveolar endocytosis?

Caveolar endocytosis is a clathrin-independent endocytic process which involves bulb-shaped, 50-60nm plasma membrane invaginations called caveolae (or ‘little caves’). Caveolae formation is driven by integral membrane proteins called caveolins as well as peripheral membrane proteins called cavins. Read more..

How do mechanical stresses regulate autophagy?

When autophagy is acting as a pro-survival mechanism primarily induced by stress, it can be naturally regulated by mechanical stresses such as compression, stretching or shear stress due to fluid flow. Consistent with this, a number of studies have highlighted how cells respond to mechanical stresses by regulating autophagy levels and how this could have implications in both physiological as well as pathophysiological conditions. Read more..

What is the physiological relevance of autophagy?

Autophagy is a both a stress-management system and a means of homeostatic control in cells, and is therefore regulated differently under varying cellular conditions. Read more..

<div class="fusion-fullwidth fullwidth-box fusion-builder-row-1-1 nonhundred-percent-fullwidth non-hundred-percent-height-scrolling" style="background-color: rgba(255,255,255,0);background-position: center center;background-repeat: no-repeat;padding-top:0px;padding-right:0px;padding-bottom:0px;padding-left:0px;margin-bottom: 0px;margin-top: 0px;border-width: 0px 0px 0px 0px;border-color:#eae9e9;border-style:solid;" > Autophagy, meaning self-eating, is an intracellular degradation system wherein unwanted cargo, such as old or damaged organelles, unneeded proteins, as well as pathogenic agents, are digested and the macromolecular contents from the digestion are released back into the cytosol. Read more..

What is Arf6-associated endocytosis?

<div class="fusion-fullwidth fullwidth-box fusion-builder-row-1-2 nonhundred-percent-fullwidth non-hundred-percent-height-scrolling" style="background-color: rgba(255,255,255,0);background-position: center center;background-repeat: no-repeat;padding-top:0px;padding-right:0px;padding-bottom:0px;padding-left:0px;margin-bottom: 0px;margin-top: 0px;border-width: 0px 0px 0px 0px;border-color:#eae9e9;border-style:solid;" > Arf6-associated endocytosis is a clathrin-independent, plasma membrane-endosomal recycling pathway, regulated by the Arf6 protein, which is a member of the Arf family of small GTPases. In this pathway, Arf6 cycles between the inactive GDP-bound state and active GTP-bound state. Read more..

How is membrane trafficking mediated by transport vesicles?

Both endocytosis and exocytosis utilize small compartments of membrane to enclose their cargo. These transport vesicles bud off from one membrane and can dynamically fuse with other membranes, or split up into smaller vesicles by fission. Residing within the interior, or lumen, of the transport vesicles, the cargo is protected from the cytoplasm. Read more..

What is membrane trafficking?

Membrane trafficking encompasses the wide variety of processes that go into the movement of cargo (typically proteins, pathogens and other macromolecules) using membrane bound transport vesicles. This transport can take place within different organelles in the same cell, or across the cell membrane to and from the extracellular environment. Read more..

How is membrane curvature generated?

Several mechanisms have been proposed to be responsible for the generation of membrane curvature. One of the mechanisms is attributed to the specific shape of the lipid group that makes up the membrane and to any changes in their distribution or symmetry. Read more..

What is membrane curvature?

Membrane curvature refers to the physical bending of membranes to accommodate various cell morphology changes as well as the formation of membrane-bound transport intermediates like spherical vesicles or tubules. Read more..

How do membrane reservoirs alter membrane tension during cell spreading?

Membrane area is very closely linked to membrane tension, cytoskeletal attachment and membrane reservoirs. During cell spreading, the initial increase in membrane area requirements are met by depleting membrane reservoirs with the morphology of large folds such as microvilli, spikes, filopodia and ruffles. Once these reservoirs are depleted, membrane tension increases and activates exocytosis as well as myosin contraction. Read more..

How do components in a lipid bilayer move?

One of the tenets of the Fluid-Mosaic membrane model is that the components of the bilayers are free to move. Using a phospholipid as an example, the first type of movement is rotational. Here the phospholipid rotates on its axis to interact with its immediate neighbours. Read more..

What is the role of membranes in mediating vesicular transport?

Another major biological role of cell membranes is in mediating vesicular transport, either during the secretory pathway when proteins are transported from the endoplasmic reticulum to target locations such as lysosomes, endosomes, the plasma membrane and into the extracellular space or during the endocytic pathway, during which proteins and other macromolecules such as nutrients, fluids are internalized into the cell from the extracellular space. Read more..

What functions does the plasma membrane perform at the interface between the cell and its environment?

Any communication or interactions between the intracellular and extracellular spaces occurs through the plasma membrane, which forms the boundary between these two regions. Read more..

What are the physiological functions of membranes?

Eukaryotic cells and their organelles are enveloped by viscoelastic layers made of lipids and proteins. These layers are generally referred to as cell membranes and when they surround the entire cell, they are specifically known as the plasma membrane. Read more..

What are membrane reservoirs?

<div class="fusion-fullwidth fullwidth-box fusion-builder-row-1-3 nonhundred-percent-fullwidth non-hundred-percent-height-scrolling" style="background-color: rgba(255,255,255,0);background-position: center center;background-repeat: no-repeat;padding-top:0px;padding-right:0px;padding-bottom:0px;padding-left:0px;margin-bottom: 0px;margin-top: 0px;border-width: 0px 0px 0px 0px;border-color:#eae9e9;border-style:solid;" > Membrane reservoirs function as membrane buffers that help redistribute membrane area when cells need to stretch or change shape and size. They are found at the cell surface as membrane superstructures varying in size from large membrane folds, to tiny membrane invaginations and caveolae… Read more…

What are plasma membranes?

<div class="fusion-fullwidth fullwidth-box fusion-builder-row-1-4 nonhundred-percent-fullwidth non-hundred-percent-height-scrolling" style="background-color: rgba(255,255,255,0);background-position: center center;background-repeat: no-repeat;padding-top:0px;padding-right:0px;padding-bottom:0px;padding-left:0px;margin-bottom: 0px;margin-top: 0px;border-width: 0px 0px 0px 0px;border-color:#eae9e9;border-style:solid;" > Plasma membranes are subcellular structures, approximately 10nm thick, that form a protective boundary around the cell as well as the cell’s organelles. They serve to both impede foreign material from entering the cell, and prevent the cellular contents from leaking out. Read more…

What is Rho-dependent IL-2 receptor endocytosis?

Internalization of transmembrane receptors was thought to occur exclusively via clathrin-mediated endocytosis (CME). However, the discovery of clathrin-independent endocytic routes, in particular, the pathway that mediates the internalization of the cytokine receptor interleukin-2 (IL-2R), raises into question the interchangeable use of the term ‘receptor-mediated endocytosis’ as a synonym for CME [1]. It has been proposed that the specific endocytic mechanism is used to describe the pathway.

A clathrin-independent pathway dependent on RhoA and regulated by PI3K

The endocytosis of the cytokine receptor IL-2R, occurs via a constitutive, clathrin and caveolae-independent, dynamin-dependent route. This pathway is dependent on the Rho small GTPase RhoA [2] and is regulated by the lipid kinase, phosphoinositide 3-kinase (PI3K) [3]. The current model for IL2-R endocytosis is as follows: 1) IL-2R activates PI3K by interacting with its regulatory p85 subunit, leading to the production of PIP3 at the membrane 2) PIP3 induces Vav2, a guanine nucleotide exchange factor (GEF) for Rac1, that activates Rac1 3) Rac1-GTP directly binds to p85 and thus is recruited to sites containing IL2-R 4) This activates the downstream target of Rac1, the p21-activated kinase1 (Pak1), which phosphorylates cortactin, promoting its association with neuronal Wiskott-Aldrich syndrome proteins (N-WASP), activating actin polymerization. [4], [5] [3] [6].

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How does Clathrin-Mediated Endocytosis (CME) become synchronized?steve2018-02-08T09:54:25+08:30

How does Clathrin-Mediated Endocytosis (CME) become synchronized?
Actin Filament Polymerization, Actin Nucleation, Clathrin-Mediated Endocytosis, Factors Influencing Actin Filament Length, Factors Regulating Acting Filament Polymerization, Membrane Dynamics, Membrane Trafficking, Plasma Membrane

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References

Doherty GJ, and McMahon HT. Mechanisms of endocytosis. Annu. Rev. Biochem. 2009; 78:857-902. [PMID: 19317650]
Lamaze C, Dujeancourt A, Baba T, Lo CG, Benmerah A, and Dautry-Varsat A. Interleukin 2 receptors and detergent-resistant membrane domains define a clathrin-independent endocytic pathway. Mol. Cell 2001; 7(3):661-71. [PMID: 11463390]
Basquin C, Malardé V, Mellor P, Anderson DH, Meas-Yedid V, Olivo-Marin J, Dautry-Varsat A, and Sauvonnet N. The signalling factor PI3K is a specific regulator of the clathrin-independent dynamin-dependent endocytosis of IL-2 receptors. J. Cell. Sci. 2013; 126(Pt 5):1099-108. [PMID: 23345407]
Grassart A, Dujeancourt A, Lazarow PB, Dautry-Varsat A, and Sauvonnet N. Clathrin-independent endocytosis used by the IL-2 receptor is regulated by Rac1, Pak1 and Pak2. EMBO Rep. 2008; 9(4):356-62. [PMID: 18344974]
Grassart A, Meas-Yedid V, Dufour A, Olivo-Marin J, Dautry-Varsat A, and Sauvonnet N. Pak1 phosphorylation enhances cortactin-N-WASP interaction in clathrin-caveolin-independent endocytosis. Traffic 2010; 11(8):1079-91. [PMID: 20444238]
Basquin C, and Sauvonnet N. Phosphoinositide 3-kinase at the crossroad between endocytosis and signaling of cytokine receptors. Commun Integr Biol 2013; 6(4):e24243. [PMID: 23986799]

What is Rho-dependent IL-2 receptor endocytosis?

What is Fast Endophilin-Mediated Endocytosis?

How does exocytosis affect cell mechanics?

What is exocytosis?

How do clathrin-coated vesicles invaginate and mature?

What causes the narrowing of clathrin-coated vesicle necks?

How do clathrin-coated pits form?

How does dynamin help in the scission of clathrin-coated vesicles?

How are clathrin-coated vesicles uncoated?

How are clathrin-coated vesicles targeted to endosomes for fusion?

What is clathrin-mediated endocytosis?

How is caveolar endocytosis mechanically regulated?

What is caveolar endocytosis?

How do mechanical stresses regulate autophagy?

What is the physiological relevance of autophagy?

What is autophagy?

What is Arf6-associated endocytosis?

How is membrane trafficking mediated by transport vesicles?

What is membrane trafficking?

How is membrane curvature generated?

What is membrane curvature?

How do membrane reservoirs alter membrane tension during cell spreading?

How do components in a lipid bilayer move?

What is the role of membranes in mediating vesicular transport?

What functions does the plasma membrane perform at the interface between the cell and its environment?

What are the physiological functions of membranes?

What are membrane reservoirs?

What are plasma membranes?

Latest Findings

How does Clathrin-Mediated Endocytosis (CME) become synchronized?

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References

What is Rho-dependent IL-2 receptor endocytosis?

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Latest Findings

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