TY - JOUR

T1 - ALG-2 oscillates in subcellular localization, unitemporally with calcium oscillations.

AU - la Cour, Jonas Marstrand

AU - Mollerup, Jens

AU - Berchtold, Martin Werner

N1 - Keywords: Adenosine Triphosphate; Apoptosis Regulatory Proteins; Calcium; Calcium Signaling; Calcium-Binding Proteins; Carrier Proteins; Cell Line, Tumor; Cytoplasm; Electrophoresis, Polyacrylamide Gel; Green Fluorescent Proteins; Hela Cells; Histamine; Humans; Immunohistochemistry; Immunoprecipitation; Microscopy, Confocal; Mutation; Protein Binding; Protein Transport; Recombinant Fusion Proteins; Time Factors; Transfection; Vesicular Transport Proteins

PY - 2007

Y1 - 2007

N2 - A variety of stimuli can trigger intracellular calcium oscillations. Relatively little is known about the molecular mechanisms decoding these events. We show that ALG-2, a Ca2+-binding protein originally isolated as a protein associated with apoptosis, is directly linked to Ca2+ signalling. We discovered that the subcellular distribution of a tagged version of ALG-2 could be directed by physiological external stimuli (including ATP, EGF, prostaglandin, histamine), which provoke intracellular Ca2+ oscillations. Cellular stimulation led to a redistribution of ALG-2 from the cytosol to a punctate localization in an oscillatory fashion unitemporally with Ca2+ oscillations, whereas a Ca2+-binding deficient mutant of ALG-2 did not redistribute. Using tagged ALG-2 as bait we identified its novel target protein Sec31A and based on the partial colocalization of endogenous ALG-2 and Sec31A we propose that ALG-2 temporarily binds to the COPII vesicles providing a link between Ca2+ signalling and ER to Golgi trafficking. Udgivelsesdato: 2007-Feb-23

AB - A variety of stimuli can trigger intracellular calcium oscillations. Relatively little is known about the molecular mechanisms decoding these events. We show that ALG-2, a Ca2+-binding protein originally isolated as a protein associated with apoptosis, is directly linked to Ca2+ signalling. We discovered that the subcellular distribution of a tagged version of ALG-2 could be directed by physiological external stimuli (including ATP, EGF, prostaglandin, histamine), which provoke intracellular Ca2+ oscillations. Cellular stimulation led to a redistribution of ALG-2 from the cytosol to a punctate localization in an oscillatory fashion unitemporally with Ca2+ oscillations, whereas a Ca2+-binding deficient mutant of ALG-2 did not redistribute. Using tagged ALG-2 as bait we identified its novel target protein Sec31A and based on the partial colocalization of endogenous ALG-2 and Sec31A we propose that ALG-2 temporarily binds to the COPII vesicles providing a link between Ca2+ signalling and ER to Golgi trafficking. Udgivelsesdato: 2007-Feb-23

U2 - 10.1016/j.bbrc.2006.12.143

DO - 10.1016/j.bbrc.2006.12.143

M3 - Journal article

C2 - 17214967

VL - 353

SP - 1063

EP - 1067

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 4

ER -