WDR35 Antibody

Product Specifications

Background

WDR35 Antibody: WD40 repeats are a common structural module in eukaryotic proteins, and proteins containing WD40 domains have a wide range of functions, including signal transduction, cell cycle regulation, RNA splicing, and transcription. One such protein, WDR35, also known as CED2, has been shown to be mutated in patients with Sensenbrenner syndrome/cranioectodermal dysplasia (CED), an autosomal-recessive disease that is characterized by craniosynstosis and ectodermal and skeletal abnormalities. WDR35 localizes to cilia and dentrosomes during embryogenesis and human and mouse fibroblasts that lack this gene fail to produce cilia. Mutations in this gene can also cause short-rib polydactyly syndromes due to abnormal ciliogenesis.

NCBI Gene ID

57539

Swiss Prot

Q9P2L0

Accession Number

NP_001006658

Host

Rabbit

Reactivity

Human

Clonality

Polyclonal

Conjugation

Unconjugated

Type

Primary Antibodies

Field of Research

Stem Cell

Purification

WDR35 Antibody is affinity chromatography purified via peptide column.

Positive Control

Cat. No. 11-701 - Human Testis Tissue Slide

Concentration

1 mg/mL

Homology

Predicted species reactivity based on immunogen sequence: Rat: (94%), Mouse: (94%)

Buffer

WDR35 Antibody is supplied in PBS containing 0.02% sodium azide.

Modification

None

Shipping Conditions

Blue Ice

Storage Conditions

WDR35 antibody can be stored at 4˚ C for three months and -20˚ C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Fragment

IgG

Specificity

WDR35 antibody is human specific.

Symbol

WDR35

NCBI Official Name

WD repeat domain 35

NCBI Organism

Homo sapiens

Background Reference 01

Gilissen C, Arts HH, Hoischen A, et al. Exome sequencing identifies WDR35 variants involded in Sensenbrenner syndrome. Am. J. Hum. Genet. 2010; 87:418-23.

Background Reference 02

Mill P, Lockhart PJ, Fitzpatrick E, et al. Human and mouse mutations in WDR35 cause short-rib polydactyly syndromes due to abnormal ciliogenesis. Am J. Hum. Genet. 2011; 88:508-15.