Vimentin is hyperphosphorylated in primary human fibroblasts treated with okadaic acid

Yatsunami; Fujiki; Suganuma; Yoshizawa; John Eriksson; Olson; Goldman

doi:10.1016/0006-291X(91)90662-Q

Vimentin is hyperphosphorylated in primary human fibroblasts treated with okadaic acid

Yatsunami
, Fujiki
, Suganuma
, Yoshizawa
, John Eriksson
, Olson
, Goldman

Forskningsoutput: Tidskriftsbidrag › Artikel › Vetenskaplig › Peer review

69 Citeringar (Scopus)

Sammanfattning

Okadaic acid and dinophysistoxin-1 (35-methylokadaic acid) induced hyperphosphorylation of a 58 kDa protein in primary human fibroblasts, due to inhibition of protein phosphatase 1 and 2A activities. The protein was present in the nuclear and cytosolic fractions. Its pI was 5.3. The hyperphosphorylated protein reacted with monoclonal and polyclonal anti-vimentin antibodies, but not with anti-nucleolin antibody. Phosphorylation of vimentin was stimulated in vitro by dinophysistoxin-1 dose-dependently in the presence of protein phosphatase 2A and protein kinases.

Originalspråk	Odefinierat/okänt
Sidor (från-till)	1165–1170
Tidskrift	Biochemical and Biophysical Research Communications
Volym	177
Nummer	3
DOI	https://doi.org/10.1016/0006-291X(91)90662-Q
Status	Publicerad - 1991
MoE-publikationstyp	A1 Tidskriftsartikel-refererad

Åtkomst av dokument

10.1016/0006-291X(91)90662-Q

Citera det här

@article{492891a246bd43e58fe18efd87129aa1,

title = "Vimentin is hyperphosphorylated in primary human fibroblasts treated with okadaic acid",

abstract = "Okadaic acid and dinophysistoxin-1 (35-methylokadaic acid) induced hyperphosphorylation of a 58 kDa protein in primary human fibroblasts, due to inhibition of protein phosphatase 1 and 2A activities. The protein was present in the nuclear and cytosolic fractions. Its pI was 5.3. The hyperphosphorylated protein reacted with monoclonal and polyclonal anti-vimentin antibodies, but not with anti-nucleolin antibody. Phosphorylation of vimentin was stimulated in vitro by dinophysistoxin-1 dose-dependently in the presence of protein phosphatase 2A and protein kinases.",

author = "Yatsunami and Fujiki and Suganuma and Yoshizawa and John Eriksson and Olson and Goldman",

year = "1991",

doi = "10.1016/0006-291X(91)90662-Q",

language = "Odefinierat/ok{\"a}nt",

volume = "177",

pages = "1165–1170",

journal = "Biochemical and Biophysical Research Communications",

issn = "0006-291X",

publisher = "Academic Press",

number = "3",

}

TY - JOUR

T1 - Vimentin is hyperphosphorylated in primary human fibroblasts treated with okadaic acid

AU - Yatsunami, null

AU - Fujiki, null

AU - Suganuma, null

AU - Yoshizawa, null

AU - Eriksson, John

AU - Olson, null

AU - Goldman, null

PY - 1991

Y1 - 1991

N2 - Okadaic acid and dinophysistoxin-1 (35-methylokadaic acid) induced hyperphosphorylation of a 58 kDa protein in primary human fibroblasts, due to inhibition of protein phosphatase 1 and 2A activities. The protein was present in the nuclear and cytosolic fractions. Its pI was 5.3. The hyperphosphorylated protein reacted with monoclonal and polyclonal anti-vimentin antibodies, but not with anti-nucleolin antibody. Phosphorylation of vimentin was stimulated in vitro by dinophysistoxin-1 dose-dependently in the presence of protein phosphatase 2A and protein kinases.

AB - Okadaic acid and dinophysistoxin-1 (35-methylokadaic acid) induced hyperphosphorylation of a 58 kDa protein in primary human fibroblasts, due to inhibition of protein phosphatase 1 and 2A activities. The protein was present in the nuclear and cytosolic fractions. Its pI was 5.3. The hyperphosphorylated protein reacted with monoclonal and polyclonal anti-vimentin antibodies, but not with anti-nucleolin antibody. Phosphorylation of vimentin was stimulated in vitro by dinophysistoxin-1 dose-dependently in the presence of protein phosphatase 2A and protein kinases.

U2 - 10.1016/0006-291X(91)90662-Q

DO - 10.1016/0006-291X(91)90662-Q

M3 - Artikel

SN - 0006-291X

VL - 177

SP - 1165

EP - 1170

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 3

ER -