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ALX4 encodes a paired-like homeodomain transcription factor expressed in the mesenchyme of developing bones, limbs, hair, teeth, and mammary tissue. Additionally we are shipping ALX4 Antibodies (58) and ALX4 Proteins (3) and many more products for this protein.
overexpression of ALX4 inhibited the proliferation, invasion, and epithelial-mesenchymal transition (EMT (show ITK ELISA Kits)) in HCC (show FAM126A ELISA Kits) cells. ALX4 had an inhibitory effect on the sonic hedgehog (Shh (show SHH ELISA Kits)) signaling pathway.
mother of Case 2 also had a mutation in the ALX4 gene, but no enlarged parietal foramina
Our results show that HOXB13 (show HOXB13 ELISA Kits)/SLUG (show SNAI2 ELISA Kits) and ALX4/SLUG (show SNAI2 ELISA Kits) axes are novel pathways that promote EMT (show ITK ELISA Kits) and invasion of ovarian cancer cells.
High-quality solution NMR structures of three homeodomains from human proteins ALX4, ZHX1 (show ZHX1 ELISA Kits) and CASP8AP2 (show CASP8AP2 ELISA Kits) were solved.
We suggest that all ALX4 heterozygote carriers be examined in detail for possible changes in nasal configuration, to establish a detailed genotype-phenotype correlation, leading the way to more comprehensive genetic counseling.
Epigenetic silencing of Aristaless-like homeobox-4 is associated with lung cancer.
study describes 2 related individuals with a heterozygous mutation in ALX4 presenting a distinct phenotype of frontonasal dysplasia; suggest that the loss of the ALX4 OAR domain with the maintenance of the homeodomain impairs the function of the normal allele in a dominant-negative effect
ALX4 variants may have an impact on the genetic etiology of nonsyndromic craniosynostosis.
Exclusion of mutations in ALX4 gene in patients with the syndrome of frontonasal dysgenesis, callosal agenesis, basal encephalocele, and eye anomalies
Downregulation of HoxB2 (show HOXB2 ELISA Kits), HoxB4 (show HOXB4 ELISA Kits) and Alx4 expression during the narrow window of early embryogenesis may cause omphalocele in the Cd chick model by interfering with molecular signaling required for proper VBW formation.
novel allele of Alx4 results in reduced Fgf10 (show FGF10 ELISA Kits) expression and failure of eyelid fusion in mice
Alx4 genetically interacts with and Shh (show SHH ELISA Kits) and Gli3 (show GLI3 ELISA Kits) during genital tubercle formation.
A mutagenesis study characterizes a polydactylous phenotype that is caused by a nonsense mutation in the Alx4 gene.
Progression of calvarial bone development requires Foxc1 (show FOXC1 ELISA Kits) regulation of Msx2 and Alx4.
the loss of the severe preaxial polydactyly characteristic of Gli3 (show GLI3 ELISA Kits)-/- limbs in double mutant embryos establishes that this type of polydactyly requires Alx4 function.
Function and regulation of Alx4 in limb development entail complex genetic interactions with Gli3 (show GLI3 ELISA Kits) and Shh (show SHH ELISA Kits).
Alx4, is required for normal branching morphogenesis of the ductal epithelia during pubescent mammary gland development.
This gene encodes a paired-like homeodomain transcription factor expressed in the mesenchyme of developing bones, limbs, hair, teeth, and mammary tissue. Mutations in this gene cause parietal foramina 2 (PFM2)\; an autosomal dominant disease characterized by deficient ossification of the parietal bones. Mutations in this gene also cause a form of frontonasal dysplasia with alopecia and hypogonadism\; suggesting a role for this gene in craniofacial development, mesenchymal-epithelial communication, and hair follicle development. Deletion of a segment of chromosome 11 containing this gene, del(11)(p11p12), causes Potocki-Shaffer syndrome (PSS)\; a syndrome characterized by craniofacial anomalies, mental retardation, multiple exostoses, and genital abnormalities in males. In mouse, this gene has been shown to use dual translation initiation sites located 16 codons apart.
aristaless-like homeobox 4
, homeobox protein aristaless-like 4
, homeodomain transcription factor ALX4
, aristaless 4
, Aristaless-like 4
, Strong's luxoid