EpsinR L10E overexpression in COS cells

Insertion of a glutamic acid (E) in place of the hydrophobic leucine (L)

is predicted to affect epsinR's ability to bend membranes

Myc-EpsinR L10E with endogenous AP1 and internalised transferrin in COS cells

Insertion of a glutamic acid (E) in place of the hydrophobic leucine (L) is predicted to affect epsinR's ability to bend membranes. This mutant is not as severe as the lipid binding mutant (D34G +R67L) in that there is co-localisation with AP1 in the perinuclear region but not with GGAs. This mutant is predicted to cause a budding defect.

Click image to view individual channels or proceed to galleries of images below.

Colocalisation of EpsinR L10E (green) with markers (red), focusing on the perinuclear region.

AP1
Large Image (62 kb)
Full field

Clathrin
Full field

GGA
Large Image (40 kb)

M6P receptor
Full field

GM130
Large Image (11 kb)

TGN46
Large Image (14 kb)

LAMP1 - Red
Large Image (51 kb)

EEA1
Large Image (71 kb)

CD63
Large Image (20 kb)

Blue - Transferrin
Large Image (53 kb)

EpsinR cover page

Endogenous epsinR expression

Comparison of epsin1 and epsinR

Myc-epsinR (WT) overexpression and colocalisation with markers

Myc-epsinR D34G+R67L (lipid binding mutant)

Myc-epsinR L10E (proposed lipid conformation mutant)

Myc-epsinR D342R+D422R (clathrin binding mutant)

Myc-epsinR D34G+R67L + D342R+D422R (lipid and clathrin binding mutant)

EpsinR-GFP and ENTH domain overexpression

EpsinR home page

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