MKRN3 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, IF, E |
---|---|
Primary Accession | Q6NSB6 |
Other Accession | NP_005655, 5032243 |
Reactivity | Human, Mouse, Rat |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | IgG |
Calculated MW | Predicted: 55 kDa Observed: 55 kDa |
Application Notes | MKRN3 antibody can be used for detection of MKRN3 by Western blot at 1 - 2 µg/mL. For immunofluorescence start at 20 µg/mL. |
Gene ID | 7681 |
---|---|
Target/Specificity | MKRN3; MKRN3 antibody is human specific. MKRN3 antibody is predicted to not cross-react with other members of the MKRN protein family. |
Reconstitution & Storage | MKRN3 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. |
Precautions | MKRN3 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
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Provided below are standard protocols that you may find useful for product applications.
Background
The Makorin ring finger 3 (MKRN3) protein contains a RING (C3HC4) zinc finger motif and several C3H zinc finger motifs. The MKRN3 gene is intronless and imprinted, with expression only from the paternal allele. Disruption of the imprinting at this locus may contribute to Prader-Willi syndrome (1), but a deletion of the gene does not (2). A deficiency of MKRN3 has been shown to cause central precocious puberty in humans (3).
References
Jong MT, Gray TA, Ji Y, et al. A novel imprinted gene, encoding a RING zinc-finger protein, a overlapping antisense transcript in the Prader-Willi syndrome critical region. Hum. Mol. Genet. 1999; 8:783-93.
Kanber D, Giltay J, Wieczorek D, et al. A paternal deletion of MKRN3, MAGEL2 and NDN does not result in Prader-Willi syndrome. Eur. J. Hum. Genet. 2009; 17:582-90.
Abreu AP, Dauber A, Macedo DB, et al. Central precocious puberty caused by mutations in the imprinting gene MKRN3. N. Engl. J. Med. 2013; 368:2467-75.
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