Introduction
YAP (Yes-associated protein) and TAZ (transcriptional coactivator with
WW and PDZ domains; WWTR1) were initially considered novel
transcriptional coactivators interacting with the TEAD family of
DNA-binding transcription factors [1]. YAP/TAZ are
replication inhibitors that promote cell proliferation, stem cell
maintenance and tissue stability[2]. YAP/TAZ acts
as a sensor for the structural and mechanical characteristics of the
cellular microenvironment [3,4]. They shuttle
between the cytoplasm and nucleus in response to multiple inputs[5]. The subcellular localization of YAP is
regulated by Ser phosphorylation (127) [6], while
the localization of YAP/TAZ is further affected by cytoskeletal
components involved in morphological changes, receptor-mediated
signaling, as well as cytoplasmic and nuclear actin[7-9]. Nuclear YAP/TAZ promotes cell
proliferation, organ overgrowth, stress survival, and postmitotic cell
dedifferentiation into their respective tissue progenitors[10]. Activation of YAP/TAZ reflects the ’social’
behavior of cells, including cell adhesion and mechanical signals
obtained by the structure of the cell organization and extracellular
pericellular tissues[4]. It is proven that
simultaneous revitalization discourse or excessive YAP/TAZ leads to the
transformation and development of the above tumor cells[11]. In contrast, MEK/MAPK inhibitors[12,13] and γ-secretase inhibitors (GSIs)[14] have the ability to actively reduce YAP/TAZ
levels. YAP/TAZ is not required for the normal physiology of most adult
organs but plays an important role in organ growth during embryonic
development and in promoting tissue repair after adult tissue injury.
Intestinal diseases are mainly inflammatory and based on tumors. YAP/TAZ
plays an important role in this process. Therefore, this article
discusses the YAP/TAZ protein connection involving the relevant sick
leave business processes and with intestinal diseases the most indicated
intestinal disease processes.
Binding of transcription factors