Anti-BHLHE40 monoclonal antibody (DCABH-10736)

Mouse anti-Human BHLHE40 monoclonal antibody for WB, sELISA, ELISA


Host Species
Antibody Isotype
Species Reactivity
Human, Mouse
BHLHB2 (NP_003661, 130 a.a. ~ 229 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.


Alternative Names
BHLHE40; basic helix-loop-helix family, member e40; basic helix loop helix domain containing, class B, 2 , BHLHB2, STRA13; class E basic helix-loop-helix protein 40; differentiated embryo chondrocyte expressed gene 1; bHLHe40
Entrez Gene ID
UniProt ID

Product Background

BMAL1:CLOCK/NPAS2 Activates Circadian Expression, organism-specific biosystem; Circadian Clock, organism-specific biosystem; Circadian rhythm - mammal, organism-specific biosystem; Circadian rhythm - mammal, conserved biosystem; Circadian rhythm pathway, organism-specific biosystem; HIF-1-alpha transcription factor network, organism-specific biosystem; HIF-2-alpha transcription factor network, organism-specific biosystem;


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We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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Circadian rhythmicity: A functional connection between differentiated embryonic chondrocyte-1 (DEC1) and small heterodimer partner (SHP)


Authors: Marczak, Marek M.; Yan, Bingfang

Circadian rhythm misalignment has been increasingly recognized to pose health risk for a wide range of diseases, particularly metabolic disorders. The liver maintains metabolic homeostasis and expresses many circadian genes, such as differentiated embryo chondrocyte-1 (DEC1) and small heterodimer partner (SHP). DEC1 is established to repress transcription through E-box elements, and SHP belongs to the superfamily of nuclear receptors and has multiple E-box elements in its promoter. Importantly, DEC1 and SHP are inversely oscillated. This study was performed to test the hypothesis that the SHP gene is a target gene of DEC1. Cotransfection demonstrated that DEC1 repressed the SHP promoter and attenuated the transactivation of the classic circadian activator complex of Clock/Bma11. Site-directed mutagenesis, electrophoretic mobility shift assay and chromatin immunoprecipitation established that the repression was achieved through the E-box in the proximal promoter. Transfection of DEC1 suppressed the expression of SHP. In circadian-inducing cells, the epileptic agent valproate inversely altered the expression of DEC1 and SHP. Both DEC1 and SHP are involved in energy balance and valproate is known to induce hepatic steatosis. Our findings collectively establish that DEC1 participates in the negative loop of SHP oscillating expression with potential implications in metabolic homeostasis. (C) 2017 Elsevier Inc. All rights reserved.

A molecular network regulating the proinflammatory phenotype of human memory T lymphocytes


Authors: Emming, Stefan; Bianchi, Niccolo; Polletti, Sara; Balestrieri, Chiara; Leoni, Cristina; Montagner, Sara; Chirichella, Michele; Delaleu, Nicolas; Natoli, Gioacchino; Monticelli, Silvia

Understanding the mechanisms that modulate helper T lymphocyte functions is crucial to decipher normal and pathogenic immune responses in humans. To identify molecular determinants influencing the pathogenicity of T cells, we separated ex vivo-isolated primary human memory T lymphocytes on the basis of their ability to produce high levels of inflammatory cytokines. We found that the inflammatory, cytokine-producing phenotype of memory T lymphocytes was defined by a specific core gene signature and was mechanistically regulated by the constitutive activation of the NF-kappa B pathway and by the expression of the transcriptional repressor BHLHE40. BHLHE40 attenuated the expression of anti-inflammatory factors, including miR-146a, a negative regulator of NF-kappa B activation and ZC3H12D, an RNase of the Regnase-1 family able to degrade inflammatory transcripts. Our data reveal a molecular network regulating the proinflammatory phenotype of human memory T lymphocytes, with the potential to contribute to disease. Monticelli and colleagues analyze primary human CD4(+) T cells to interrogate gene expression regulatory pathways that distinguish GM-CSF+ pathogenic programs from noninflammatory programs. They identify the transcriptional repressor BHLHE40 as an enforcer of proinflammatory gene expression by suppressing the NF-kappa B inhibitor miR-146a and the RNase ZC3H12D.

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