Product Name	Anti-SIX1/AP
Chinese Name	碱性磷酸酶（AP）标记的同源盒蛋白SIX1抗体
Alias	BOS3; DFNA23; Homeobox protein SIX1; OTTHUMP00000179042; Sine oculis homeobox homolog 1; SIX homeobox 1; SIX1; SIX1_HUMAN; TIP39.
Research Area	Cell biology  Developmental biology  transcriptional regulatory factor  Epigenetics
Immunogen Species	Rabbit
Clonality	Polyclonal
React Species	(predicted: Human, Mouse, Rat, Cow, Rabbit, Sheep, )
Applications	WB=1:50-200 IHC-P=1:50-200 IHC-F=1:50-200 ICC=1:50-200  not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
Molecular weight	32kDa
Form	Lyophilized or Liquid
Concentration	1mg/ml
immunogen	KLH conjugated synthetic peptide derived from human SIX1
Lsotype	IgG
Purification	affinity purified by Protein A
Storage Buffer	0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage	Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
Product Detail	background: The protein encoded by this gene is a homeobox protein that is similar to the Drosophila 'sine oculis' gene product. This gene is found in a cluster of related genes on chromosome 14 and is thought to be involved in limb development. Defects in this gene are a cause of autosomal dominant deafness type 23 (DFNA23) and branchiootic syndrome type 3 (BOS3). [provided by RefSeq, Jul 2008] Function: May be involved in limb tendon and ligament development. Subcellular Location: Nucleus. Tissue Specificity: Specifically expressed in skeletal muscle. DISEASE: Defects in SIX1 are the cause of deafness autosomal dominant type 23 (DFNA23) [MIM:605192]. A form of non-syndromic deafness characterized by prelingual, bilateral, symmetric hearing loss with a conductive component present in some but not all patients. Defects in SIX1 are the cause of branchiootic syndrome type 3 (BOS3) [MIM:608389]. BOS3 is a syndrome characterized by usually bilateral branchial cleft fistulas or cysts, sensorineural and/or conductive hearing loss, pre-auricular pits, and structural defects of the outer, middle or inner ear. Otic defects include malformed and hypoplastic pinnae, a narrowed external ear canal, bulbous internal auditory canal, stapes fixation, malformed and hypoplastic cochlea. Branchial and otic anomalies are as those seen in individuals with the branchiootorenal syndrome. However, renal anomalies are absent in branchiootic syndrome patients. Note=Defects in SIX1 could be a cause of branchiootorenal syndrome (BOR). BOR is an autosomal dominant disorder manifested by various combinations of preauricular pits, branchial fistulae or cysts, lacrimal duct stenosis, hearing loss, structural defects of the outer, middle, or inner ear, and renal dysplasia. Associated defects include asthenic habitus, long narrow facies, constricted palate, deep overbite, and myopia. Hearing loss may be due to mondini type cochlear defect and stapes fixation. Penetrance of BOR syndrome is high, although expressivity can be extremely variable. Similarity: Belongs to the SIX/Sine oculis homeobox family. Contains 1 homeobox DNA-binding domain. Database links: Entrez Gene: 6495 Human Entrez Gene: 20471 Mouse Entrez Gene: 114634 Rat Omim: 601205 Human SwissProt: Q15475 Human SwissProt: Q62231 Mouse SwissProt: Q8BSP4 Mouse Unigene: 54416 Human Unigene: 713114 Human Unigene: 4645 Mouse Unigene: 23396 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

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