Datasheet

Biological Description

Specificity	ATF1 Antibody [H17A19] detects endogenous levels of total ATF1 protein.
Background	ATF1, a member of the ATF/CREB bZIP transcription factor family, is widely expressed in tissues such as the brain and endocrine organs. It forms homodimers or heterodimers (e.g., with CREB1, Fos, Jun) through its C-terminal leucine zipper domain, enabling binding to CRE/ATF sites (TGACGTCA) in target gene promoters and driving stress-responsive transcription. ATF1 contains an N-terminal activation domain rich in serine and threonine residues that serve as phosphorylation sites, most notably Ser63, which is phosphorylated by PKA to enhance CRE binding and promote coactivator (CBP/p300) recruitment. The adjacent basic DNA-binding region and leucine zipper support dimerization and DNA interaction. Post-translational modifications, including Thr184 (a Pin1 binding motif that modulates stability and activity) and Ser198 (phosphorylated by HIPK2 for repression), further regulate ATF1 function. ATF1 integrates cAMP/PKA and MAPK/ERK signaling pathways to mediate cellular adaptation, regulating genes such as c-fos and BDNF involved in proliferation, differentiation, survival, and stress responses (e.g., H2O2-inducible gpd1/ctt1). At promoters, ATF1 acts as a nucleosome barrier, establishing nucleosome-depleted regions, phasing downstream nucleosomes, and suppressing cryptic and antisense transcription. It fine-tunes homeostasis under genotoxic and oxidative stress by competing with histones at CRE sites, thereby maintaining chromatin organization and preventing nucleosome disorganization within coding regions. Pin1-mediated cis-trans isomerization at phosphorylated Thr184 enhances ATF1’s oncogenic potential. ATF1 is implicated in diseases including clear cell sarcoma (where EWSR1-ATF1 fusions hyperactivate MITF via CRE, driving oncogenesis), other cancers (where upregulation promotes growth and survival through synergy with AP-1), and neurodegenerative disorders (where disrupted CREB/ATF2 crosstalk impairs neuronal stress responses).

Specificity

ATF1 Antibody [H17A19] detects endogenous levels of total ATF1 protein.

Background

ATF1, a member of the ATF/CREB bZIP transcription factor family, is widely expressed in tissues such as the brain and endocrine organs. It forms homodimers or heterodimers (e.g., with CREB1, Fos, Jun) through its C-terminal leucine zipper domain, enabling binding to CRE/ATF sites (TGACGTCA) in target gene promoters and driving stress-responsive transcription. ATF1 contains an N-terminal activation domain rich in serine and threonine residues that serve as phosphorylation sites, most notably Ser63, which is phosphorylated by PKA to enhance CRE binding and promote coactivator (CBP/p300) recruitment. The adjacent basic DNA-binding region and leucine zipper support dimerization and DNA interaction. Post-translational modifications, including Thr184 (a Pin1 binding motif that modulates stability and activity) and Ser198 (phosphorylated by HIPK2 for repression), further regulate ATF1 function. ATF1 integrates cAMP/PKA and MAPK/ERK signaling pathways to mediate cellular adaptation, regulating genes such as c-fos and BDNF involved in proliferation, differentiation, survival, and stress responses (e.g., H2O2-inducible gpd1/ctt1). At promoters, ATF1 acts as a nucleosome barrier, establishing nucleosome-depleted regions, phasing downstream nucleosomes, and suppressing cryptic and antisense transcription. It fine-tunes homeostasis under genotoxic and oxidative stress by competing with histones at CRE sites, thereby maintaining chromatin organization and preventing nucleosome disorganization within coding regions. Pin1-mediated cis-trans isomerization at phosphorylated Thr184 enhances ATF1’s oncogenic potential. ATF1 is implicated in diseases including clear cell sarcoma (where EWSR1-ATF1 fusions hyperactivate MITF via CRE, driving oncogenesis), other cancers (where upregulation promotes growth and survival through synergy with AP-1), and neurodegenerative disorders (where disrupted CREB/ATF2 crosstalk impairs neuronal stress responses).

Usage Information

Application

WB, IP, IHC, IF, FCM

Dilution

WB	IP	IHC	IF	FCM
1:1000	1:50	1:100	1:100	1:150

Reactivity

Mouse, Rat, Human

Source

Rabbit Monoclonal Antibody

MW

29 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

References

https://pubmed.ncbi.nlm.nih.gov/25122751/
https://pubmed.ncbi.nlm.nih.gov/8414969/

ATF1 Antibody [H17A19]

Biological Description

Usage Information

References

Application Data