Anti-ATF2 (Ser490,498) Antibody
Our Anti-ATF2 (Ser490,498) rabbit polyclonal phosphospecific primary antibody from PhosphoSolutions
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, IHC |
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Primary Accession | P15336 |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | IgG |
Calculated MW | 54537 Da |
Gene ID | 1386 |
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Other Names | Activating transcription factor 2 antibody, Activating transcription factor 2 splice variant ATF2 var2 antibody, ATF 2 antibody, Atf-2 antibody, Atf2 antibody, ATF2 protein antibody, ATF2_HUMAN antibody, cAMP Response Element Binding Protein 2 antibody, cAMP response element binding protein CRE BP1 antibody, cAMP response element-binding protein CRE-BP1 antibody, cAMP responsive element binding protein 2, formerly antibody, cAMP-dependent transcription factor ATF-2 antibody, cAMP-responsive element-binding protein 2 antibody, CRE BP1 antibody, CRE-BP antibody, CREB 2 antibody, CREB-2 antibody, CREB2 antibody, CREBP1 antibody, Cyclic AMP dependent transcription factor ATF 2 antibody, Cyclic AMP-dependent transcription factor ATF-2 antibody, Cyclic AMP-responsive element-binding protein 2 antibody, D130078H02Rik antibody, D18875 antibody, HB 16 antibody, HB16 antibody, Histone acetyltransferase ATF2 antibody, MGC105211 antibody, MGC105222 antibody, MGC111558 antibody, MGC142504 antibody, mXBP antibody, MXBP protein antibody, Tg(Gzma-Klra1)7Wum antibody, TREB 7 antibody, TREB7 antibody |
Target/Specificity | The activating transcription factor ATF2 (also called CRE-BP1) binds to both AP-1 and CRE DNA response elements and is a member of the ATF/CREB family of leucine zipper proteins (Maekawa et al., 1989). ATF2 has been implicated in the transcriptional regulation of a number of genes including cytokines, cell cycle control and apoptosis. Various forms of cellular stress, including inflammatory cytokines and UV irradiation, stimulate the transcriptional activity of ATF2 (Ivanov et al., 2003; Morton et al., 2004). Stress induced ATFdependent transcription is dependent on phosphorylation of ATF (Fuchs et al., 2000); Morton et al., 2004). Serine 490 and serine 498 are novel phosphorylation sites on ATF that have recently been identified. ATF2 is particularly abundant in the brain and the ATF2 family of transcription factors is considered an important substrate of signals upstream of the activation of genes associated with neuronal growth and differentiation (Karin and Hunter, 1995). ATF expression has also been linked to the depression in humans (Laifenfeld et al., 2004). |
Format | Antigen Affinity Purified from Pooled Serum |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | Anti-ATF2 (Ser490,498) Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Shipping | Blue Ice |
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Provided below are standard protocols that you may find useful for product applications.
Background
The activating transcription factor ATF2 (also called CRE-BP1) binds to both AP-1 and CRE DNA response elements and is a member of the ATF/CREB family of leucine zipper proteins (Maekawa et al., 1989). ATF2 has been implicated in the transcriptional regulation of a number of genes including cytokines, cell cycle control and apoptosis. Various forms of cellular stress, including inflammatory cytokines and UV irradiation, stimulate the transcriptional activity of ATF2 (Ivanov et al., 2003; Morton et al., 2004). Stress induced ATFdependent transcription is dependent on phosphorylation of ATF (Fuchs et al., 2000); Morton et al., 2004). Serine 490 and serine 498 are novel phosphorylation sites on ATF that have recently been identified. ATF2 is particularly abundant in the brain and the ATF2 family of transcription factors is considered an important substrate of signals upstream of the activation of genes associated with neuronal growth and differentiation (Karin and Hunter, 1995). ATF expression has also been linked to the depression in humans (Laifenfeld et al., 2004).
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