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Rabbit anti-Human ATF6 Polyclonal Antibody

The antibody against ATF6 was raised in Rabbit using the recombinant fusion protein containing a sequence corresponding to amino acids 190-300 of human ATF6 (NP_031374.2) as the immunogen. The polyclonal antibody exists as a isotype IgG, by affinity purification. This antibody has been validated on WB, IHC-P, IF/ICC, ELISA.

ADA-13045A

The antibody against ATF6 was raised in Rabbit using the recombinant fusion protein containing a sequence corresponding to amino acids 190-300 of human ATF6 (NP_031374.2) as the immunogen. The polyclonal antibody exists as a isotype IgG, by affinity purification. This antibody has been validated on WB, IHC-P, IF/ICC, ELISA.

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Specifications


Cat.No ADA-13045A ClonalityPolyclonal
Host SpeciesRabbitTarget NameATF6
Target SynonymsACHM7; ATF6A; ATF6FormLiquid
Species ReactivityHuman, Mouse, RatIsotypeIgG
Storage Buffer50% Glycerol, PBS with 0.05% proclin300, pH7.3.Purification MethodAffinity purification
Positive SamplesRat lungApplicationELISA, WB, IF/ICC, IHC-P

Immunogen Information


Immunogen DescriptionRecombinant fusion protein containing a sequence corresponding to amino acids 190-300 of human ATF6 (NP_031374.2).Target SpeciesHuman
Immunogen SequencePKTQTNSSVPAKTIIIQTVPTLMPLAKQQPIISLQPAPTKGQTVLLSQPTVVQLQAPGVLPSAQPVLAVAGGVTQLPNHVVNVVPAPSANSPVNGKLSVTKPVLQSTMRNVUniprot IDP18850
Background Information
  • Uniprot Id

    P18850

  • Target Species

    Human

  • Target Name

    ATF6

  • Target Full Name

    Cyclic AMP-dependent transcription factor ATF-6 alpha

  • Target Function

    Precursor of the transcription factor form (Processed cyclic AMP-dependent transcription factor ATF-6 alpha), which is embedded in the endoplasmic reticulum membrane. Endoplasmic reticulum stress promotes processing of this form, releasing the transcription factor form that translocates into the nucleus, where it activates transcription of genes involved in the unfolded protein response (UPR).; Transcription factor that initiates the unfolded protein response (UPR) during endoplasmic reticulum stress by activating transcription of genes involved in the UPR. Binds DNA on the 5'-CCAC[GA]-3'half of the ER stress response element (ERSE) (5'-CCAAT-N(9)-CCAC[GA]-3') and of ERSE II (5'-ATTGG-N-CCACG-3'). Binding to ERSE requires binding of NF-Y to ERSE. Could also be involved in activation of transcription by the serum response factor. May play a role in foveal development and cone function in the retina.

  • Target Involvement

    Achromatopsia 7 (ACHM7)

  • Target Subcellular Location

    Endoplasmic reticulum membrane; Single-pass type II membrane protein. Golgi apparatus membrane; Single-pass type II membrane protein.; [Processed cyclic AMP-dependent transcription factor ATF-6 alpha]: Nucleus.

  • Target Protein Families

    BZIP family, ATF subfamily

  • Target Tissue Specificity

    Ubiquitous.

  • Target Synonyms

    ATF6; Cyclic AMP-dependent transcription factor ATF-6 alpha; cAMP-dependent transcription factor ATF-6 alpha; Activating transcription factor 6 alpha; ATF6-alpha

  • Target Background

    This gene encodes a transcription factor that activates target genes for the unfolded protein response (UPR) during endoplasmic reticulum (ER) stress. Although it is a transcription factor, this protein is unusual in that it is synthesized as a transmembrane protein that is embedded in the ER. It functions as an ER stress sensor/transducer, and following ER stress-induced proteolysis, it functions as a nuclear transcription factor via a cis-acting ER stress response element (ERSE) that is present in the promoters of genes encoding ER chaperones. This protein has been identified as a survival factor for quiescent but not proliferative squamous carcinoma cells. There have been conflicting reports about the association of polymorphisms in this gene with diabetes in different populations, but another polymorphism has been associated with increased plasma cholesterol levels. This gene is also thought to be a potential therapeutic target for cystic fibrosis.

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