Associative memory plays a role in ER-1α positive breast cancers.
TL;DR
This perspective brings together multiple observations concerning the regulatory architecture and functional interactions of the TP53 gene and its isoforms to cooperate to maintain an open chromatin state in the P2 region in a manner reminiscent of a neural "associative memory" network.
Abstract
This perspective brings together multiple observations concerning the regulatory architecture and functional interactions of the TP53 gene and its isoforms. The TP53 gene encompasses an internal enhancer-promoter region (P2) located between exons 2 and 5, which is transactivated by full-length TAp53α, to drive the expression of truncated TP53 isoforms ΔN133p53α, β or γ. ΔN133p53α homo-monomers or dimers very likely form hetero-tetramers with homo-dimers of full-length TAp53α. The TAp53α-ΔN133p53 tetramer then acts as a transcription factor augmenting mitochondrial efficiency, DNA repair, telomere restoration and reversing cellular senescence, thus opposing many outputs of tumor suppressive TAp53α homo-tetramers. Other transcription factors, such as estrogen receptor (ER), OCT1, and SOX9 also may bind the P2 promoter-enhancer to promote transcription of oncogenic TP53 isoforms. These transcription factors, together with full-length TAp53α, appear to cooperate to maintain an open chromatin state in the P2 region in a manner reminiscent of a neural "associative memory" network.