ATF-3 Antibody [D14J2] | Primary Antibodies

Application: Reactivity: Human, Mouse

Usage Information

Dilution
WB1:1000 IP1:100 IF1:100 - 1:400 FCM1:400 - 1:1600 CHIP1:50

Application
WB, IP, IF, FCM, ChIP

Reactivity
Human, Mouse

Source
Rabbit Monoclonal Antibody

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

Predicted MW
23 kDa, 24 kDa

Positive Control	HCT 116 cells; RAW 264.7 cells; 293 T cells; BeWo cells
Negative Control	NIH/3T3 cells; MCF7 cells; A172 cells

Datasheet & SDS

Biological Description

Specificity
ATF-3 Antibody [D14J2] detects endogenous levels of total ATF-3 protein.

Clone
D14J2

Synonym(s)
Cyclic AMP-dependent transcription factor ATF-3; cAMP-dependent transcription factor ATF-3; Activating transcription factor 3; ATF3

Background
ATF3 (activating transcription factor 3) is a stress-inducible member of the ATF/CREB bZIP transcription factor family, encoded by a gene with four exons that produces a 181-amino-acid protein. It functions as a multifunctional hub in cellular adaptive responses by forming homo- or heterodimers to either repress or activate target genes depending on the cellular context. ATF3 contains an N-terminal acidic transactivation domain rich in Asp and Glu residues for coactivator recruitment, a central basic DNA-binding region that recognizes ATF/CRE consensus sites such as TGACGTCA, and a C-terminal leucine zipper for dimerization, characterized by heptad repeats with hydrophobic leucines at the ‘d’ positions. Key post-translational modifications, like SUMOylation at Lys42, enhance protein stability and proliferation, while flexible linker regions provide conformational adaptability. ATF3 integrates a variety of stress signals, including cytokines, genotoxins, UV radiation, and cAMP, primarily via AP-1, NF-κB, and JNK pathways, to transcriptionally repress pro-inflammatory genes (such as IL-6, TNF-α, and MMP-1 in macrophages), promote cell survival (by repressing Bak/Bax after TLR activation), and modulate metabolism and immunity. Formation of heterodimers with JunB or c-Fos amplifies gene inhibition, whereas homodimerization confers gene repression. ATF3 fine-tunes the resolution of inflammation, regulates macrophage polarization (M1/M2 balance through Wnt/β-catenin signaling), maintains apoptosis equilibrium, and modulates oncogenesis, acting as a tumor suppressor in skin and lung cancers by reducing proliferation, or as an oncogene in breast cancer and glioma by increasing chemoresistance through ABCB1/m6A mechanisms. Its disease relevance encompasses atherosclerosis (where it is repressed by FOXP3 in regulatory T cells), various cancers (including tamoxifen resistance via YTHDF2), autoimmunity, and neurodegeneration, with its expression regulated by mRNA stabilizers such as HuR/Egr-1 and microRNAs like 27b-3p.

Background

ATF3 (activating transcription factor 3) is a stress-inducible member of the ATF/CREB bZIP transcription factor family, encoded by a gene with four exons that produces a 181-amino-acid protein. It functions as a multifunctional hub in cellular adaptive responses by forming homo- or heterodimers to either repress or activate target genes depending on the cellular context. ATF3 contains an N-terminal acidic transactivation domain rich in Asp and Glu residues for coactivator recruitment, a central basic DNA-binding region that recognizes ATF/CRE consensus sites such as TGACGTCA, and a C-terminal leucine zipper for dimerization, characterized by heptad repeats with hydrophobic leucines at the ‘d’ positions. Key post-translational modifications, like SUMOylation at Lys42, enhance protein stability and proliferation, while flexible linker regions provide conformational adaptability. ATF3 integrates a variety of stress signals, including cytokines, genotoxins, UV radiation, and cAMP, primarily via AP-1, NF-κB, and JNK pathways, to transcriptionally repress pro-inflammatory genes (such as IL-6, TNF-α, and MMP-1 in macrophages), promote cell survival (by repressing Bak/Bax after TLR activation), and modulate metabolism and immunity. Formation of heterodimers with JunB or c-Fos amplifies gene inhibition, whereas homodimerization confers gene repression. ATF3 fine-tunes the resolution of inflammation, regulates macrophage polarization (M1/M2 balance through Wnt/β-catenin signaling), maintains apoptosis equilibrium, and modulates oncogenesis, acting as a tumor suppressor in skin and lung cancers by reducing proliferation, or as an oncogene in breast cancer and glioma by increasing chemoresistance through ABCB1/m6A mechanisms. Its disease relevance encompasses atherosclerosis (where it is repressed by FOXP3 in regulatory T cells), various cancers (including tamoxifen resistance via YTHDF2), autoimmunity, and neurodegeneration, with its expression regulated by mRNA stabilizers such as HuR/Egr-1 and microRNAs like 27b-3p.

References
https://pubmed.ncbi.nlm.nih.gov/32922364/ https://pubmed.ncbi.nlm.nih.gov/19705082/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%