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ACAD-11 Polyclonal Antibody

Product code: YP-Ab-02462
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Product introduction

Reactive species
Human;Rat;Mouse;
Applications
WB;IHC;IF;ELISA
Antibody type
Polyclonal Antibody
Gene Name
ACAD11
Protein name
Acyl-CoA dehydrogenase family member 11
Dalton(DA)
87kD
Immunogen
The antiserum was produced against synthesized peptide derived from human ACAD11. AA range:381-430
Specificity
ACAD-11 Polyclonal Antibody detects endogenous levels of ACAD-11 protein.
Constitute
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source
Polyclonal, Rabbit,IgG
Dilution rate
WB: 1/500 - 1/2000. IHC: 1/100 - 1/300. ELISA: 1/20000.. IF 1:50-200
Purification process
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration
1 mg/ml
Stockpile
-20°C/1 year
Other name
ACAD11; Acyl-CoA dehydrogenase family member 11; ACAD-11
Background
acyl-CoA dehydrogenase family member 11(ACAD11) Homo sapiens This gene encodes an acyl-CoA dehydrogenase enzyme with a preference for carbon chain lengths between 20 and 26. Naturally occurring read-through transcription occurs between the upstream gene NPHP3 (nephronophthisis 3 (adolescent)) and this gene. [provided by RefSeq, Aug 2015],
Function
alternative products:Additional isoforms seem to exist,disease:Defects in NPHP3 are a cause of renal-hepatic-pancreatic dysplasia (RHPD) [MIM:208540]. RHPD is an autosomal recessive disorder with variable expression, and patients surviving the neonatal period progress to renal and hepatic failure which can be treated successfully with combined liver-kidney transplantation.,disease:Defects in NPHP3 are the cause of nephronophthisis type 3 (NPHP3) [MIM:604387]; also known as adolescent nephronophthisis. NPHP3 is a autosomal recessive disorder resulting in end-stage renal disease. It is characterized by polyuria, polydipsia, anemia. Onset of terminal renal failure occurr significantly later (median age, 19 years) than in juvenile nephronophthisis. Renal pathology is characterized by alterations of tubular basement membranes, tubular atrophy and dilatation, sclerosing tubulointerstitial neph

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