Anti-ETHE1 Antibody

Product Name

Anti-ETHE1 Antibody

View all ETHE1 Antibodies

SKU/Catalog Number

A05557

Size

100ul

Form

Liquid

Description

Boster Bio Anti-ETHE1 Antibody catalog # A05557. Tested in WB,IHC,ICC/IF applications. This antibody reacts with Human,Mouse,Rat.

Storage & Handling

Store at -20°C for one year. For short term storage and frequent use, store at 4°C for up to one month. Avoid repeated freeze-thaw cycles.

Cite This Product

Anti-ETHE1 Antibody (Boster Biological Technology, Pleasanton CA, USA, Catalog # A05557)

Host

Rabbit

Contents

Rabbit IgG, 1mg/ml in PBS with 0.02% sodium azide, 50% glycerol, pH7.2

Clonality

Polyclonal

Isotype

IgG

Immunogen

Synthesized peptide derived from human MSK2 around the phosphorylation site of T568.

*Blocking peptide can be purchased. Costs vary based on immunogen length. Contact us for pricing.

Reactive Species

A05557 is reactive to ETHE1 in Human, Mouse, Rat

Applications

A05557 is guaranteed for IF, IHC, ICC, WB Boster Guarantee

Observed Molecular Weight

111 kDa

Calculated molecular weight

27.873kDa

Background of ETHE1

Serine/threonine-protein kinase that is required for the mitogen or stress-induced phosphorylation of the transcription factors CREB1 and ATF1 and for the regulation of the transcription factor RELA, and that contributes to gene activation by histone phosphorylation and functions in the regulation of inflammatory genes. Phosphorylates CREB1 and ATF1 in response to mitogenic or stress stimuli such as UV-C irradiation, epidermal growth factor (EGF) and anisomycin. Plays an essential role in the control of RELA transcriptional activity in response to TNF. Phosphorylates 'Ser-10' of histone H3 in response to mitogenics, stress stimuli and EGF, which results in the transcriptional activation of several immediate early genes, including proto-oncogenes c-fos/FOS and c-jun/JUN. May also phosphorylate 'Ser-28' of histone H3. Mediates the mitogen- and stress-induced phosphorylation of high mobility group protein 1 (HMGN1/HMG14). In lipopolysaccharide-stimulated primary macrophages, acts downstream of the Toll-like receptor TLR4 to limit the production of pro-inflammatory cytokines. Functions probably by inducing transcription of the MAP kinase phosphatase DUSP1 and the anti-inflammatory cytokine interleukin 10 (IL10), via CREB1 and ATF1 transcription factors.

Pierrat B.,J. Biol. Chem. 273:29661-29671(1998).
Deak M.,EMBO J. 17:4426-4441(1998).
Soloaga A.,EMBO J. 22:2788-2797(2003).<

Antibody Validation

Boster validates all antibodies on WB, IHC, ICC, Immunofluorescence, and ELISA with known positive control and negative samples to ensure specificity and high affinity, including thorough antibody incubations.

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Assay Dilutions Recommendation

The recommendations below provide a starting point for assay optimization. The actual working concentration varies and should be decided by the user.

WB: 1:200-1:1000
IHC: 1:50-1:200
ICC/IF: 1:50-1:200

Validation Images & Assay Conditions

There are currently no images for this product. We are working on uploading them please check back shortly or contact us to expedite our upload process for this antibody.

Gene/Protein Information For ETHE1 (Source: Uniprot.org, NCBI)

Alternative Names

D83198; EC 3.1.2.6; ethylmalonic encephalopathy 1; Ethylmalonic encephalopathy protein 1; Hepatoma subtracted clone one protein; HSCOEC 3.-; protein ETHE1, mitochondrial; YF13H12 ETHE1 HSCO, YF13H12 ETHE1 persulfide dioxygenase persulfide dioxygenase ETHE1, mitochondrial|ethylmalonic encephalopathy 1|hepatoma subtracted clone one protein|protein ETHE1, mitochondrial|sulfur dioxygenase ETHE1

For more info on ETHE1, check out the ETHE1 Infographic

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In this infographic, you will see the following information for ETHE1: database IDs, superfamily, protein function, synonyms, molecular weight, chromosomal locations, tissues of expression, subcellular locations, post-translational modifications, and related diseases, research areas & pathways. If you want to see more information included, or would like to contribute to it and be acknowledged, please contact [email protected].

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