NFYA

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Template:Short description Template:Use dmy dates Template:Cs1 config Template:Infobox gene Nuclear transcription factor Y subunit alpha is a protein that in humans is encoded by the NFYA gene.[1][2]

Function

The protein encoded by this gene is one subunit of a trimeric complex NF-Y, forming a highly conserved transcription factor that binds to CCAAT motifs in the promoter regions in a variety of genes.[3] Subunit NFYA associates with a tight dimer composed of the NFYB and NFYC subunits, resulting in a trimer that binds to DNA with high specificity and affinity. The sequence specific interactions of the complex are made by the NFYA subunit, suggesting a role as the regulatory subunit. In addition, there is evidence of post-transcriptional regulation in this gene product, either by protein degradation or control of translation. Further regulation is represented by alternative splicing in the glutamine-rich activation domain, with clear tissue-specific preferences for the two isoforms.[4]

NF-Y complex serves as a pioneer factor by promoting chromatin accessibility to facilitate other co-localizing cell type-specific transcription factors.[5]

NF-Y has also been implicated as a central player in transcription start site (TSS) selection in animals.[6] It safeguards the integrity of the nucleosome-depleted region and PIC localization at protein-coding gene promoters.

Interactions

NFYA has been shown to interact with Serum response factor[7] and ZHX1.[7][8] NFYA, NFYB and NFYC form the NFY complex and it has been shown that the NFY complex serves as a pioneer factor by promoting chromatin accessibility to facilitate other co-localizing cell type-specific transcription factors.[3]

Structure

The atomic structure of the NFY heterotrimer in complex with dsDNA was resolved via X-ray crystallography (PDB ID 4awl).[9] Using one of the NFYA alpha helices as a template, structure inspired stapled peptides were designed to disrupt the NFY heterotrimer formation by preventing NFYA from binding to the NFYB/C heterodimer.[10]

References

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Further reading

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External links

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

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