Role of Zeb2/Sip1 in neuronal development

Epifanova, Ekaterina A.; Бабаев, А.А.; Newman, Andrew G.; Tarabykin, Victor

doi:10.1016/j.brainres.2018.09.034

Cited by 49 publications

(51 citation statements)

References 66 publications

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“…Zinc-finger E-box binding homeobox 2 (ZEB2) is a ubiquitous transcription factor that plays critical roles in TGF-β, and Bone Morphogenetic Protein (BMP) signaling pathways [123,124]. It is also crucial in embryonic development [125] and the development of the neural crest [126,127]. ZEB2 has two zinc finger clusters that bind to CACCT sequences and inhibit transcription [128,129].…”

Section: Zinc-finger E-box Binding Homeoboxmentioning

confidence: 99%

Host Transcription Factors in Hepatitis B Virus RNA Synthesis

Turton

Meier-Stephenson

Badmalia

et al. 2020

Viruses

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The hepatitis B virus (HBV) chronically infects over 250 million people worldwide and is one of the leading causes of liver cancer and hepatocellular carcinoma. HBV persistence is due in part to the highly stable HBV minichromosome or HBV covalently closed circular DNA (cccDNA) that resides in the nucleus. As HBV replication requires the help of host transcription factors to replicate, focusing on host protein–HBV genome interactions may reveal insights into new drug targets against cccDNA. The structural details on such complexes, however, remain poorly defined. In this review, the current literature regarding host transcription factors’ interactions with HBV cccDNA is discussed.

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Section: Zinc-finger E-box Binding Homeoboxmentioning

confidence: 99%

Host Transcription Factors in Hepatitis B Virus RNA Synthesis

Turton

Meier-Stephenson

Badmalia

et al. 2020

Viruses

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“…The very low sensitivity of the components that represent ETS1, LEF1, and ZEB2 is in accordance with the importance that of the three transcription factors not only during EndMT, but also during other cell differentiation processes. Specifically, ZEB2 is involved in T cell differentiation (Goossens et al, 2019) and neurological development (Epifanova et al, 2018). LEF1 is important during osteogenesis (Li et al, 2018), immune cell regulation (Chae and Bothwell, 2018), and hair follicle development (Abaci et al, 2018).…”

Section: Robustness Analysismentioning

confidence: 99%

“…Experimentally, the loss of SNAI2 (Niessen et al, 2008), TWIST1 (Mammoto et al, 2018), or ZEB1 (Sanchez-Tillo et al, 2010 prevents EndMT. ZEB2 has many functions in addition to its role during EndMT, its loss causes severe neurodevelopmental defects and cardiovascular malformations (Epifanova et al, 2018), while its specific effect during EndMT still needs to be elucidated. Conversely, the gain of ZEB2 function is sufficient to trigger EndMT (DaSilva-Arnold et al, 2018).…”

Section: The Model As Theoretical Frameworkmentioning

confidence: 99%

A Computational Model of the Endothelial to Mesenchymal Transition

2020

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Endothelial cells (ECs) form the lining of lymph and blood vessels. Changes in tissue requirements or wounds may cause ECs to behave as tip or stalk cells. Alternatively, they may differentiate into mesenchymal cells (MCs). These processes are known as EC activation and endothelial-to-mesenchymal transition (EndMT), respectively. EndMT, Tip, and Stalk EC behaviors all require SNAI1, SNAI2, and Matrix metallopeptidase (MMP) function. However, only EndMT inhibits the expression of VE-cadherin, PECAM1, and VEGFR2, and also leads to EC detachment. Physiologically, EndMT is involved in heart valve development, while a defective EndMT regulation is involved in the physiopathology of cardiovascular malformations, congenital heart disease, systemic and organ fibrosis, pulmonary arterial hypertension, and atherosclerosis. Therefore, the control of EndMT has many promising potential applications in regenerative medicine. Despite the fact that many molecular components involved in EC activation and EndMT have been characterized, the system-level molecular mechanisms involved in this process have not been elucidated. Toward this end, hereby we present Boolean network model of the molecular involved in the regulation of EC activation and EndMT. The simulated dynamic behavior of our model reaches fixed and cyclic patterns of activation that correspond to the expected EC and MC cell types and behaviors, recovering most of the specific effects of simple gain and loss-of-function mutations as well as the conditions associated with the progression of several diseases. Therefore, our model constitutes a theoretical framework that can be used to generate hypotheses and guide experimental inquiry to comprehend the regulatory mechanisms behind EndMT. Our main findings include that both the extracellular microevironment and the pattern of molecular activity within the cell regulate EndMT. EndMT requires a lack of VEGFA and sufficient oxygen in the extracellular microenvironment as well as no FLI1 and GATA2 activity within the cell. Additionally Tip cells cannot undergo EndMT directly. Furthermore, the specific conditions that are sufficient to trigger EndMT depend on the specific pattern of molecular activation within the cell.

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“…In vertebrates, the ZEB transcription factors are important throughout the development and differentiation of many cell lineages, such as the haematopoietic lineage [ 48 , 49 ]. The ZEBs have been shown to be crucial mainly during the formation of neural crest cells (NCCs) and their subsequent differentiation into their various derivatives, such as the neurogenic lineage and melanocyte lineage [ 50 , 51 ]. Neural crest cells are motile and give rise to many different cell types, including melanocytes, craniofacial bone and cartilage, peripheral neurons and glial cells, adipose tissue, cardiac smooth muscle cells and secretory adrenal glands.…”

Section: Zebs During Specification From Neural Crest Cells Towardsmentioning

confidence: 99%

Intrinsic Balance between ZEB Family Members Is Important for Melanocyte Homeostasis and Melanoma Progression

Bruneel

Verstappe

Vandamme

et al. 2020

Cancers

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It has become clear that cellular plasticity is a main driver of cancer therapy resistance. Consequently, there is a need to mechanistically identify the factors driving this process. The transcription factors of the zinc-finger E-box-binding homeobox family, consisting of ZEB1 and ZEB2, are notorious for their roles in epithelial-to-mesenchymal transition (EMT). However, in melanoma, an intrinsic balance between ZEB1 and ZEB2 seems to determine the cellular state by modulating the expression of the master regulator of melanocyte homeostasis, microphthalmia-associated transcription factor (MITF). ZEB2 drives MITF expression and is associated with a differentiated/proliferative melanoma cell state. On the other hand, ZEB1 is correlated with low MITF expression and a more invasive, stem cell-like and therapy-resistant cell state. This intrinsic balance between ZEB1 and ZEB2 could prove to be a promising therapeutic target for melanoma patients. In this review, we will summarise what is known on the functional mechanisms of these transcription factors. Moreover, we will look specifically at their roles during melanocyte-lineage development and homeostasis. Finally, we will overview the current literature on ZEB1 and ZEB2 in the melanoma context and link this to the ‘phenotype-switching’ model of melanoma cellular plasticity.

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Role of Zeb2/Sip1 in neuronal development

Cited by 49 publications

References 66 publications

Host Transcription Factors in Hepatitis B Virus RNA Synthesis

Host Transcription Factors in Hepatitis B Virus RNA Synthesis

A Computational Model of the Endothelial to Mesenchymal Transition

Intrinsic Balance between ZEB Family Members Is Important for Melanocyte Homeostasis and Melanoma Progression

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