Rabbit Anti-ADAR1/FITC Conjugated antibody

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136kDa double stranded RNA binding protein; Adar 1; ADAR; Adar1; Adenosine deaminase RNA specific 1; Adenosine deaminase RNA specific; Adenosine deaminase that act on RNA; AV242451; Double stranded RNA specific adenosine deaminase; Double-stranded RNA-spe

Cat:

SL2168R-FITC

Species Reactivity：

Human,Mouse,Rat,

Immunogen：

KLH conjugated synthetic peptide derived from human DRADA

Format：

Lyophilized or Liquid

Storage instructions：

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 ant

Buffer：

0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.

Concentration：

1mg/ml

Clonality：

Polyclonal

Isotype：

IgG

Applications：

IF=1:50-200not yet tested in other applications.optimal dilutions/concentrations should be determined by the end user.

Host：

Rabbit

Calculated MW：

135kDa

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Unit:

Price: $596.00

Product PDFs

Datasheet: Down Datasheet

Other Information
Citations
Protein Attributes
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background:
This gene encodes the enzyme responsible for RNA editing by site-specific deamination of adenosines. This enzyme destabilizes double-stranded RNA through conversion of adenosine to inosine. Mutations in this gene have been associated with dyschromatosis symmetrica hereditaria. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jul 2010]

Function:
Converts multiple adenosines to inosines and creates I/U mismatched base pairs in double-helical RNA substrates without apparent sequence specificity. Has been found to modify more frequently adenosines in AU-rich regions, probably due to the relative ease of melting A/U base pairs as compared to G/C pairs. Functions to modify viral RNA genomes and may be responsible for hypermutation of certain negative-stranded viruses. Edits the messenger RNAs for glutamate receptor (GLUR) subunits by site-selective adenosine deamination. Produces low-level editing at the GLUR-B Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Binds to short interfering RNAs (siRNA) without editing them and suppresses siRNA-mediated RNA interference. Binds to ILF3/NF90 and up-regulates ILF3-mediated gene expression.

Subunit:
Homodimer. Isoform 1 interacts with ILF2/NF45 and ILF3/NF90.

Subcellular Location:
Cytoplasm. Nucleus, nucleolus. Isoform 1: Cytoplasm. Note=Found predominantly in cytoplasm but appears to shuttle between the cytoplasm and nucleus. Isoform 5: Nucleus, nucleolus.

Tissue Specificity:
Ubiquitously expressed, highest levels were found in brain and lung.

Post-translational modifications:
Sumoylation reduces RNA-editing activity.

DISEASE:
Defects in ADAR are a cause of dyschromatosis symmetrical hereditaria (DSH) [MIM:127400]; also known as reticulate acropigmentation of Dohi. DSH is a pigmentary genodermatosis of autosomal dominant inheritance characterized by a mixture of hyperpigmented and hypopigmented macules distributed on the dorsal parts of the hands and feet.

Similarity:
Contains 1 A to I editase domain.
Contains 2 DRADA repeats.
Contains 3 DRBM (double-stranded RNA-binding) domains.

Database links:

Entrez Gene: 103 Human

Entrez Gene: 56417 Mouse

Omim: 146920 Human

SwissProt: P55265 Human

SwissProt: Q99MU3 Mouse

Unigene: 12341 Human

Unigene: 679967 Human

Unigene: 316628 Mouse

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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