Map Key
Generic Enzyme
Generic kinase
Protein kinase
Lipid kinase
Generic phosphatase
Protein phosphatase
Lipid phosphatase
Generic phospholipase
Generic protease
RAS - superfamily
G beta/gamma
Regulators (GDI, GAP, GEF)
Generic channel
Ligand-gated channel
Voltage-gated channel
Normal process
Pathological process
Positive effect
Negative effect
Unspecified effect
Technical link
Disrupts in disease
Emerges in disease
Enhances in disease
Weakens in disease
Organsim specific interaction

Generic binding protein
Receptor ligand
Cell membrane glycoprotein
Transcription factor
Inorganic ion
Predicted metabolite or user's structure
Generic receptor
Receptors with enzyme activity

Normal process
Pathological process
Covalent modifications
Transcription regulation
MicroRNA binding
Influence on expression
Unspecified interactions
Pharmacological effect
Toxic effect
Group relation
Complex subunit
Similarity reaction
A complex or a group
Organism specific object

Clathrin-dependent protein traffic

Log In to Post A Comment

Clathrin-dependent protein traffic

Clathrin-dependent protein traffic

Transport vesicles are classified according to the components of the protein coat thatsurrounds them during their genesis and early life. One of the most common and probablybest-characterized classes of coated vesicles are Clathrin -coated vesicles (CCVs)that cotain three protein layers. CCVs are so-called because the main component of thecoat is Clathrin, a complex that forms a polymeric mechanical scaffold on thevesicle surface. The inner, membrane layer with its embedded cargo is linked to the outerClathrin layer by a middle layer that consists of various clathrin-adaptormolecules and other proteins that have accessory/regulatory roles in CCV assembly.Classical key components of the absolute majority of the cargos in Clathrin-dependentendocytosis are Adaptor-related protein complex 2 ( AP complex 2 ) [1], [2], [3].

After the Clathrin lattice is formed, dynamins (e.g., Dynamin-2 ),endophilins (e.g., Endophilin B1 ), epsins and amphiphysins (e.g., BIN1 )are involved in membrane invagination and Clathrin rearrangements. The plus-endmotor Myosin I pulls the Dynamin-2 ring in the direction of the cellsurface, while the minus-end motor Myosin VI pulls the coated bud into thecytosol. The resulting strain could then sever the constricted stalk beneath the dynaminring [4].

Next phase is a fusion of coated-pit-derived primary endocytic vesicles with sortingendosomes. It is regulated by member RAS oncogene family Rab-5A, Early endosomeantigen 1 ( EEA1 ) [5], [6], [7] andSoluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNARE) [7], [8].

The maturation of sorting endosomes to late endosomes is realized with participationmember RAS oncogene family Rab7 via unknown mechanism [9], [10].

Late endosomes fusion to each other or to lysosomes via SNARE-mediated mechanism[11], [12], [8].

In addition, Rab7 is directly involved in the aggregation and fusion of lateendocytic structures/lysosomes [11], [13].

Subsequently, cargo is delivered to the Golgi from late endosomes with participationof RAS oncogene family Rab-9 [10], [14], [15].In addition, proteins from endoplasmic reticulum may be translocated to the Golgi in Coatprotein complex-II ( COPII )-dependent manner [16].

Modified in endoplasmic reticulum and/or Golgi, the cargo may be delivered from theGolgi back to the cell surface, possibly with participation of Rab8/Optineurin/ Myosin VI pathway [7], [17], [18] and/or coat protein complex termed Coatomer [19], [7], [20].

Moreover, cargo may be delivered to the cell surface via a short pathway fromendosomes via different recycling endosomes [7]. The latter is realizedmainly via Rab-4 and/or Rab-11A -dependent mechanisms [10],[21], [22].

It is shown, that recycling endosomes to the Golgi may be realized via different SNAREcomplexes [23], [7], [8].