Microcephalin and pericentrin regulate mitotic entry via centrosome-associated Chk1
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Microcephalin and pericentrin regulate mitotic entry via centrosome-associated Chk1. / Tibelius, Alexandra; Marhold, Joachim; Zentgraf, Hanswalter; Heilig, Christoph E; Neitzel, Heidemarie; Ducommun, Bernard; Rauch, Anita; Ho, Anthony D; Bartek, Jiri; Krämer, Alwin.
In: Journal of Cell Biology, Vol. 185, No. 7, 2009, p. 1149-57.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Microcephalin and pericentrin regulate mitotic entry via centrosome-associated Chk1
AU - Tibelius, Alexandra
AU - Marhold, Joachim
AU - Zentgraf, Hanswalter
AU - Heilig, Christoph E
AU - Neitzel, Heidemarie
AU - Ducommun, Bernard
AU - Rauch, Anita
AU - Ho, Anthony D
AU - Bartek, Jiri
AU - Krämer, Alwin
N1 - Keywords: Animals; Antigens; Cell Line; Centrosome; Cyclin B; Enzyme Activation; Humans; Microcephaly; Mitosis; Nerve Tissue Proteins; Protein Kinases; RNA Interference; cdc25 Phosphatases
PY - 2009
Y1 - 2009
N2 - Primary microcephaly, Seckel syndrome, and microcephalic osteodysplastic primordial dwarfism type II (MOPD II) are disorders exhibiting marked microcephaly, with small brain sizes reflecting reduced neuron production during fetal life. Although primary microcephaly can be caused by mutations in microcephalin (MCPH1), cells from patients with Seckel syndrome and MOPD II harbor mutations in ataxia telangiectasia and Rad3 related (ATR) or pericentrin (PCNT), leading to disturbed ATR signaling. In this study, we show that a lack of MCPH1 or PCNT results in a loss of Chk1 from centrosomes with subsequently deregulated activation of centrosomal cyclin B-Cdk1.
AB - Primary microcephaly, Seckel syndrome, and microcephalic osteodysplastic primordial dwarfism type II (MOPD II) are disorders exhibiting marked microcephaly, with small brain sizes reflecting reduced neuron production during fetal life. Although primary microcephaly can be caused by mutations in microcephalin (MCPH1), cells from patients with Seckel syndrome and MOPD II harbor mutations in ataxia telangiectasia and Rad3 related (ATR) or pericentrin (PCNT), leading to disturbed ATR signaling. In this study, we show that a lack of MCPH1 or PCNT results in a loss of Chk1 from centrosomes with subsequently deregulated activation of centrosomal cyclin B-Cdk1.
U2 - 10.1083/jcb.200810159
DO - 10.1083/jcb.200810159
M3 - Journal article
C2 - 19546241
VL - 185
SP - 1149
EP - 1157
JO - Journal of Cell Biology
JF - Journal of Cell Biology
SN - 0021-9525
IS - 7
ER -
ID: 18697925