ArticleMolecular and cellular biology2004
Loss of the Sall3 gene leads to palate deficiency, abnormalities in cranial nerves, and perinatal lethality.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 63 citations in OpenAlex.
- Loss of 18q Alters TGFβ Signalling Affecting Anteroposterior Neuroectodermal Fate in Human Embryonic Stem Cells.Cell proliferation · 2025Article
- Identification of Pappa and Sall3 as Gli3 direct target genes acting downstream of cilia signaling in corticogenesis.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Relating enhancer genetic variation across mammals to complex phenotypes using machine learning.Science (New York, N.Y.) · 2023Article
- Structure of SALL4 zinc finger domain reveals link between AT-rich DNA binding and Okihiro syndrome.Life science alliance · 2023Article
- A developmental pathway for epithelial-to-motoneuron transformation in C. elegans.Cell reports · 2022Article
- SALL Proteins; Common and Antagonistic Roles in Cancer.Cancers · 2021Review
- Analysis of FGF20-regulated genes in organ of Corti progenitors by translating ribosome affinity purification.Developmental dynamics : an official publication of the American Association of Anatomists · 2020Article
- SALL3 expression balance underlies lineage biases in human induced pluripotent stem cell differentiation.Nature communications · 2019Article
- Chimeric NANOG repressors inhibit glioblastoma growth in vivo in a context-dependent manner.Scientific reports · 2019Article
- Epigenetic modification ofJournal of Cancer · 2018Article
- Effect of siRNA-silencing of SALL2 gene on growth, migration and invasion of human ovarian carcinoma A2780 cells.BMC cancer · 2017Article
- IL-7Rα glutamylation and activation of transcription factor Sall3 promote group 3 ILC development.Nature communications · 2017Article
- Copy number variants in a population-based investigation of Klippel-Trenaunay syndrome.American journal of medical genetics. Part A · 2017Article
- Epigenetic silencing ofClinical epigenetics · 2017Article
- Ring chromosome 18 in combination with 18q12.1 (DTNA) interstitial microdeletion in a patient with multiple congenital defects.Molecular cytogenetics · 2016Article
- Molecular basis of cleft palates in mice.World journal of biological chemistry · 2015Review
- The tumor suppressor protein p150(Sal2) in carcinogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- Aberrant Hypermethylation of SALL3 with HPV Involvement Contributes to the Carcinogenesis of Cervical Cancer.PloS one · 2015Article
- Aberrant methylation and downregulation of sall3 in human hepatocellular carcinoma.World journal of gastroenterology · 2012Article
- Sall1 regulates cortical neurogenesis and laminar fate specification in mice: implications for neural abnormalities in Townes-Brocks syndrome.Disease models & mechanisms · 2012Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Members of the Spalt gene family encode putative transcription factors characterized by seven to nine C2H2 zinc finger motifs. Four genes have been identified in mice--Spalt1 to Spalt4 (Sall1 to Sall4). Spalt homologues are widely expressed in neural and mesodermal tissues during early embryogenesis. Sall3 is normally expressed in mice from embryonic day 7 (E7) in the neural ectoderm and primitive streak and subsequently in the brain, peripheral nerves, spinal cord, limb buds, palate, heart, and otic vesicles. We have generated a targeted disruption of Sall3 in mice. Homozygous mutant animals die on the first postnatal day and fail to feed. Examination of the oral structures of these animals revealed that abnormalities were present in the palate and epiglottis from E16.5. In E10.5 embryos, deficiencies in cranial nerves that normally innervate oral structures, particularly the glossopharyngeal nerve (IX), were observed. These studies indicate that Sall3 is required for the development of nerves that are derived from the hindbrain and for the formation of adjacent branchial arch derivatives.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.