SKU: WP12899 Categories: ,

KALIG-1 Polyclonal Antibody

Price range: $268.00 through $328.00

SKU: WP12899-100
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Product details

Background:

Mutations in this gene cause the X-linked Kallmann syndrome. The encoded protein is similar in sequence to proteins known to function in neural cell adhesion and axonal migration. In addition, this cell surface protein is N-glycosylated and may have anti-protease activity. [provided by RefSeq, Jul 2008],

Specifications

Size50μL/100μL
TargetKALIG-1
ReactivityHuman
ApplicationsWB, IHC
MW(Calculated)
MW(Observed)76kD
Host SpeciesRabbit
IsotypeIgG
Conjugate/ModificationUnmodified
Recommended Dilution RatioWB 1:500-2000; IHC 1:50-300 / Note: For IHC, we suggest antigen retrieval with TE buffer pH 9.0 (Cat#WT1004)
FormulationLiquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
PurificationThe antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Storage-15°C to -25°C/1 year(Do not lower than -25°C)
Concentration1 mg/ml
ClonalityPolyclonal
Clone Number
ImmunogenThe antiserum was produced against synthesized peptide derived from human KAL1. AA range:151-200
SpecificityKALIG-1 Polyclonal Antibody detects endogenous levels of KALIG-1 protein.
Gene NameKAL1
Protein NameAnosmin-1
Other NameKAL1; / ADMLX; / KAL; / KALIG1; / Anosmin-1; / Adhesion molecule-like X-linked; / Kallmann syndrome protein
SpeciesHuman
Gene ID3730
UniprotP23352
Species.1
Gene ID.1
Uniprot.1
Species.2
Gene ID.2
Uniprot.2
Cellular LocalizationCell membrane; Peripheral membrane protein . Secreted . Proteolytic cleavage may release it from the cell surface into the extracellular space.
Tissue ExpressionExpressed in the cerebellum (at protein level).
Signaling_pathway
Research Areas
FunctionDisease:Defects in KAL1 are the cause of Kallmann syndrome type 1 (KAL1) [MIM:308700]; also known as hypogonadotropic hypogonadism and anosmia. Anosmia or hyposmia is related to the absence or hypoplasia of the olfactory bulbs and tracts. Hypogonadism is due to deficiency in gonadotropin-releasing hormone and probably results from a failure of embryonic migration of gonadotropin-releasing hormone-synthesizing neurons. In some patients other developmental anomalies can be present, which include renal agenesis, cleft lip and/or palate, selective tooth agenesis, and bimanual synkinesis. In some cases anosmia may be absent or inconspicuous.,Function:May be an adhesion-like molecule with anti-protease activity.,PTM:N-glycosylated.,similarity:Contains 1 WAP domain.,similarity:Contains 4 fibronectin type-III domains.,
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