Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Smad-interacting protein-1 (Zfhx1b) acts upstream of Wnt signaling in the mouse hippocampus and controls its formation.

Proceedings of the National Academy of Sciences of the United States of America - 31 Jul 2007

Miquelajauregui Amaya, Van de Putte Tom, Polyakov Alexander, Nityanandam Anjana, Boppana Sridhar, Seuntjens Eve, Karabinos Anton, Higashi Yujiro, Huylebroeck Danny, Tarabykin Victor

Abstract excerpt

Smad-interacting protein-1 (Sip1) [Zinc finger homeobox (Zfhx1b)] is a transcription factor implicated in the genesis of Mowat-Wilson syndrome in humans. Sip1 expression in the dorsal telencephalon of mouse embryos was documented from E12.5. We inactivated the gene specifically in cortical precursors. This resulted in the lack of the entire hippocampal formation. Sip1 mutant mice exhibited death of...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Hippocampus
Share to Intercellular Signaling Peptides and Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to JNK Mitogen-Activated Protein Kinases

Share to Stem Cells

Share to Telencephalon

Share to Up-Regulation

Share to Wnt Proteins

Share to Zinc Finger E-box Binding Homeobox 2

Source

Open in PubMed Open full text

Identifiers

PMID: 17644613
DOI: 10.1073/pnas.0609863104
PMCID: PMC1929013

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Smad-interacting protein-1 (Zfhx1b) acts upstream of Wnt signaling in the mouse hippocampus and controls its formation.PMID 17644613Read ↗

Atypical Mowat-Wilson patient confirms the importance of the novel association between ZFHX1B/SIP1 and NuRD corepressor complexSemantic proximity Read ↗

Zebrafish sip1a and sip1b are essential for normal axial and neural patterning.Semantic proximity Read ↗

Genome-wide analysis of N1ICD/RBPJ targets in vivo reveals direct transcriptional regulation of Wnt, SHH, and hippo pathway effectors by Notch1.Semantic proximity Read ↗

Mice lacking ZFHX1B, the gene that codes for Smad-interacting protein-1, reveal a role for multiple neural crest cell defects in the etiology of Hirschsprung disease-mental retardation syndrome.Semantic proximity Read ↗

Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation.Semantic proximity Read ↗

Loss-of-function mutations in SIP1 Smad interacting protein 1 result in a syndromic Hirschsprung disease.Semantic proximity Read ↗

Complementary expression pattern of Zfhx1 genes Sip1 and deltaEF1 in the mouse embryo and their genetic interaction revealed by compound mutants.Semantic proximity Read ↗

The expression of twisted gastrulation in postnatal mouse brain and functional implications.Semantic proximity Read ↗

Sip-1 mutations cause disturbances in the activity of NMDA- and AMPA-, but not kainate receptors of neurons in the cerebral cortex.Semantic proximity Read ↗

The N-terminus zinc finger domain of Xenopus SIP1 is important for neural induction, but not for suppression of Xbra expression.Semantic proximity Read ↗

The facial neural crest controls fore- and midbrain patterning by regulating Foxg1 expression through Smad1 activity.Semantic proximity Read ↗

Generation of the floxed allele of the SIP1 (Smad-interacting protein 1) gene for Cre-mediated conditional knockout in the mouse.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.