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