Smad-interacting protein-1 (Zfhx1b) acts upstream of Wnt signaling in the mouse hippocampus and controls its formation
EXPRESSION
Telencephalon
brain
knockout
hirschsprung-disease
Apoptosis
Hippocampus
mowat-wilson-syndrome
Mice
03 medical and health sciences
mental retardation syndrome
E-CADHERIN
expression
Animals
BRAIN
gene
Promoter Regions, Genetic
development
Cell Proliferation
Homeodomain Proteins
0303 health sciences
MUTATIONS
sfrp1
Stem Cells
MOWAT-WILSON-SYNDROME
sip1
JNK Mitogen-Activated Protein Kinases
Gene Expression Regulation, Developmental
Membrane Proteins
HIRSCHSPRUNG-DISEASE
mutations
GENE
Up-Regulation
Repressor Proteins
Wnt Proteins
BINDING-PROTEIN
cortex
Gene Expression Regulation
binding-protein
Mutation
SIP1
Intercellular Signaling Peptides and Proteins
MENTAL RETARDATION SYNDROME
e-cadherin
Gene Deletion
telencephalon
Signal Transduction
DOI:
10.1073/pnas.0609863104
Publication Date:
2007-07-21T00:48:49Z
AUTHORS (10)
ABSTRACT
Smad-interacting protein-1 (Sip1) [Zinc finger homeobox (Zfhx1b)] is a transcription factor implicated in the genesis of Mowat–Wilson syndrome humans. Sip1 expression dorsal telencephalon mouse embryos was documented from E12.5. We inactivated gene specifically cortical precursors. This resulted lack entire hippocampal formation. mutant mice exhibited death differentiating cells and decreased proliferation region prospective hippocampus dentate gyrus. The Wnt antagonist Sfrp1 ectopically activated, whereas activity noncanonical effector, JNK, down-regulated embryonic mice. In cells, protein detected on promoter both genes showed mutually exclusive pattern suggesting that negatively regulated by Sip1. therefore essential to development gyrus, able modulate signaling these regions.
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CITATIONS (74)
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