BHLHE41

[10][11] Klaus-Armin Nave's lab identified BHLHE41/SHARP1 and BHLHE40/SHARP2 as a novel subfamily in the basic helix-loop-helix (BHLH) protein family.

[13] After the identification of the BHLHE41 gene, Dr. Ken-Ichi Honma's lab characterized its role as a regulator in the mammalian circadian clock.

BHLHE41 is a member of the DEC subfamily within the basic helix-loop-helix (bHLH) proteins gene family.

BHLHE41-001 contains 5 coding exons, has a transcript length of 3,837 base pairs, and encodes the 482 amino acid BHLHE41 protein.

[23] The basic helix-loop-helix domain allows members of the protein family to dimerize with each other to affect gene transcription through binding to specific DNA sequences.

[24] BHLHE41 protein also has alanine and glycine-rich regions in the C-terminal, and lacks the WRPW motif for interaction with the corepressor Groucho.

[14] The gene encodes for a transcription factor that belongs to the Hairy/Enhancer of Split (Hes) subfamily of basic helix-loop-helix factor genes which encode transcriptional repressors that function as downstream targets to regulate cell fate during tissue development.

BHLHE41 knockout mice, also known as BHLHE41 -/- or BHLHE41 null, showed no change in their free-running period with respect to activity.

After being exposed to an in vivo model of allergic asthma, BHLHE41 knockout mice show decreased TH2 cytokine production, defective TH2 responses after being repeatedly stimulated with OVA peptide, and reduced alveolar infiltrate.

G9a then catalyzes repressive histone 3 lysine 9 dimethylation (H3K9me2) at promoter sites of target genes of MyoD.

[33] It has been shown that the normal tissue adjacent to colon carcinomas show high levels of BHLHE41 expression.

[35] Studies have shown that BHLHE41 is both required and sufficient to limit the expression of HIF-target genes, by mechanistically binding to HIFs and promoting proteasomal degradation.

[35] Breast cancer tumors that show high expression of BHLHE41 and CyclinG2 are believed to have a lower metastatic risk.

[36][37]This article incorporates text from the United States National Library of Medicine, which is in the public domain.