WBmore details Unsuitable for:
Flow Cyt,ICC/IF,IHC-P or IP
Mouse, Rat, Human
Synthetic peptide within Human VANGL1 aa 200-300 (internal sequence) (Cysteine residue). The exact sequence is proprietary. Database link: Q8TAA9
MCF7, HeLa, Jurkat and MOLT4 cell lysates.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents
We are constantly working hard to ensure we provide our customers with best in class antibodies. As a result of this work we are pleased to now offer this antibody in purified format. We are in the process of updating our datasheets. The purified format is designated 'PUR' on our product labels. If you have any questions regarding this update, please contact our Scientific Support team.
This product is a recombinant rabbit monoclonal antibody.
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Accordiing to PubMed:11956595, ubiquitously expressed. According to PubMed:12011995, expressed specifically in testis and ovary.
Involvement in disease
Defects in VANGL1 are a cause of neural tube defects (NTD) [MIM:182940]. NTD are congenital malformations. The most common forms of NTD are described as open defects (including anencephaly and myelomeningocele, or spina bifida), which result from the failure of fusion in the cranial and spinal region of the neural tube, respectively. Other open dysraphisms (including myeloschisis, hemimyelomeningocele, and hemimyelocele) are sometimes associated with a Chiari type 2 malformation. A number of skin-covered (closed) NTD are categorized clinically depending on the presence of a subcutaneous mass (lipomyeloschisis, lipomyelomeningocele, meningocele, and myelocystocele) or the absence of such a mass (complex dysraphic states, including split cord malformations, dermal sinus, caudal regression, and segmental spinal dysgenesis). Defects in VANGL1 are a cause of sacral defect with anterior meningocele (SDAM) [MIM:600145]. SDAM is a form of caudal dysgenesis. It is present at birth and becomes symptomatic later in life, usually because of obstructive labor in females, chronic constipation, or meningitis. Inheritance is autosomal dominant.