Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Gene Ontology annotation of human sequence-specific DNA binding transcription factors (DbTFs) based on the TFClass database
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Towards a proteome-scale map of the human protein-protein interaction network.
ALX1 induces snail expression to promote epithelial-to-mesenchymal transition and invasion of ovarian cancer cells.
Impact of cytosine methylation on DNA binding specificities of human transcription factors.
A reference map of the human binary protein interactome.
Human Cart-1: structural organization, chromosomal localization, and functional analysis of a cartilage-specific homeodomain cDNA.
Human CART1, a paired-class homeodomain protein, activates transcription through palindromic binding sites.
Prenatal folic acid treatment suppresses acrania and meroanencephaly in mice mutant for the Cart1 homeobox gene.
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Mouse Cart1 deficiency disrupts forebrain mesenchymal survival and cranial closure; this does not establish a neuron-maturation step or folate-binding activity.
"Cart1 is required for forebrain mesenchyme
survival"
P300/CBP acts as a coactivator to cartilage homeoprotein-1 (Cart1), paired-like homeoprotein, through acetylation of the conserved lysine residue adjacent to the homeodomain.
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Cart1 physically couples to p300/CBP, which enhances its transcriptional activity through acetylation. The abstract does not resolve the full donor construct and host details.
"Cart1 binds to p300 in vivo and in
vitro"
Disruption of ALX1 causes extreme microphthalmia and severe facial clefting: expanding the spectrum of autosomal-recessive ALX-related frontonasal dysplasia.
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An independent human ALX1 splice-site family corroborates the developmental disease association beyond the multigene deletion family; no direct DNA-binding assay is inferred.
"In the second family we identified a homozygous
donor-splice-site mutation (c.531+1G > A) in the ALX1 gene"
ALX1-related frontonasal dysplasia results from defective neural crest cell development and migration.
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The patient iPSC-derived neural crest cell model shows altered state and migration, but its precise developmental stage remains uncertain; the study does not establish neuronal maturation.
"a lack of understanding which stage of development the NCC represent."
Alx1 Deficient Mice Recapitulate Craniofacial Phenotype and Reveal Developmental Basis of ALX1-Related Frontonasal Dysplasia.
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Mouse Alx1 exon-2 deletion causes craniofacial skeletal defects, supporting the existing broad developmental assertion. The remaining N-terminal protein is distinguished from intact Alx1.
"embryos had hypoplastic premaxilla and presphenoid bone, and malformed palatal processes"
DNA-guided transcription factor cooperativity shapes face and limb mesenchyme.
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Endogenous tagged human ALX1 occupies regulatory chromatin in H9-derived cranial neural crest cells. Purified structure and EMSA measurements in the same study use ALX4 domains.
"However, the strength of ChIP signal is reproducibly distinct between the tagged HD TFs, with strongest signal for ALX1."
The ALX1 transcription factor acts in the early cranial mesoderm to specify extraocular muscle formation.
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Lineage-restricted mouse Alx1 deletion establishes an early cranial mesoderm requirement for extraocular muscle formation, distinct from neural crest control of muscle organization and attachment.
"ALX1 is required in the cranial mesoderm for EOM formation"
ALX1 research and annotation review