Application Note
*Optimal dilutions/concentrations should be determined by the researcher.
Application |
Recommended Dilution |
1:500-1:20000 |
1:100-1:1000 |
1:100-1:1000 |
Not tested in other applications.
Calculated MW
Positive Control
mouse liver , PC-12 , Rat-2
Predict Reactivity
Bovine(>80% identity)
Form
Liquid
Buffer
1XPBS pH7, 20% Glycerol
Preservative
0.025% ProClin 300
Storage
Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.
Concentration
1.01 mg/ml (Please refer to the vial label for the specific concentration.)
Antigen Species
Human
Immunogen
Recombinant protein encompassing a sequence within the center region of human PEX19. The exact sequence is proprietary.
Purification
Purified by antigen-affinity chromatography.
Conjugation
Unconjugated
RRID
AB_1951172
Note
For laboratory research use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Purchasers shall not, and agree not to enable third parties to, analyze, copy, reverse engineer or otherwise attempt to determine the structure or sequence of the product.
Synonyms
peroxisomal biogenesis factor 19 , D1S2223E , HK33 , PBD12A , PMP1 , PMPI , PXF , PXMP1
Cellular Localization
Cytoplasm , Peroxisome membrane; Lipid-anchor; Cytoplasmic side
Background
This gene is necessary for early peroxisomal biogenesis. It acts both as a cytosolic chaperone and as an import receptor for peroxisomal membrane proteins (PMPs). Peroxins (PEXs) are proteins that are essential for the assembly of functional peroxisomes. The peroxisome biogenesis disorders (PBDs) are a group of genetically heterogeneous autosomal recessive, lethal diseases characterized by multiple defects in peroxisome function. The peroxisomal biogenesis disorders are a heterogeneous group with at least 14 complementation groups and with more than 1 phenotype being observed in cases falling into particular complementation groups. Although the clinical features of PBD patients vary, cells from all PBD patients exhibit a defect in the import of one or more classes of peroxisomal matrix proteins into the organelle. Defects in this gene are a cause Zellweger syndrome (ZWS). [provided by RefSeq]
Database
Research Area