Human Gene WNT7A (ENST00000285018.5) from GENCODE V44
Description: Homo sapiens Wnt family member 7A (WNT7A), mRNA. (from RefSeq NM_004625) RefSeq Summary (NM_004625): This gene is a member of the WNT gene family, which consists of structurally related genes that encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene is involved in the development of the anterior-posterior axis in the female reproductive tract, and also plays a critical role in uterine smooth muscle pattering and maintenance of adult uterine function. Mutations in this gene are associated with Fuhrmann and Al-Awadi/Raas-Rothschild/Schinzel phocomelia syndromes. [provided by RefSeq, Jul 2008]. Gencode Transcript: ENST00000285018.5 Gencode Gene: ENSG00000154764.6 Transcript (Including UTRs) Position: hg38 chr3:13,816,258-13,880,071 Size: 63,814 Total Exon Count: 4 Strand: - Coding Region Position: hg38 chr3:13,818,944-13,879,816 Size: 60,873 Coding Exon Count: 4
ID:WNT7A_HUMAN DESCRIPTION: RecName: Full=Protein Wnt-7a; Flags: Precursor; FUNCTION: Ligand for members of the frizzled family of seven transmembrane receptors. Probable developmental protein. Signaling by Wnt-7a allows sexually dimorphic development of the mullerian ducts (By similarity). SUBUNIT: Interacts with PORCN (By similarity). SUBCELLULAR LOCATION: Secreted, extracellular space, extracellular matrix. TISSUE SPECIFICITY: Expression is restricted to placenta, kidney, testis, uterus, fetal lung, and fetal and adult brain. PTM: Palmitoylation at Ser-206 is required for efficient binding to frizzled receptors. It is also required for subsequent palmitoylation at Cys-73. Palmitoylation is necessary for proper trafficking to cell surface (By similarity). DISEASE: Defects in WNT7A are the cause of limb pelvis hypoplasia aplasia syndrome (LPHAS) [MIM:276820]. A syndrome of severe deficiency of the extremities due to hypo- or aplasia of one or more long bones of one or more limbs. Pelvic manifestations include hip dislocation, hypoplastic iliac bone and aplastic pubic bones. Thoracic deformity, unusual facies and genitourinary anomalies can be present. DISEASE: Defects in WNT7A are a cause of Fuhrmann syndrome (FUHRS) [MIM:228930]; also known as fibular aplasia or hypoplasia femoral bowing and poly- syn- and oligodactyly. Fuhrmann syndrome is a distinct limb-malformation disorder characterized also by various degrees of limb aplasia/hypoplasia and joint dysplasia. SIMILARITY: Belongs to the Wnt family. WEB RESOURCE: Name=GeneReviews; URL="http://www.ncbi.nlm.nih.gov/sites/GeneTests/lab/gene/WNT7A";
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on O00755
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.