TTF-1/NKX2.1 up-regulates the in vivo transcription of  nestin

Pelizzoli, Roberta; Tacchetti, Carlo; Luzzi, Paola; Strangio, Antonella; Bellese, Grazia; Zappia, Emanuela; Guazzi, Stefania

doi:10.1387/ijdb.062196rp

Cited by 11 publications

(5 citation statements)

References 31 publications

(35 reference statements)

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“…The 320-bp minimal enhancer contains several putative ciselements, such as HRE and binding sites for Sox and the POU family transcription factors (24,27,44,45). By carefully examining this sequence, we also found two overlapping binding sites for the steroidogenic factor-1 (SF1, also known as Ad4BP and NR5A1), which are in perfect agreement with the consensus sequence for SF1 (Fig.…”

Section: The Second Intron Of the Mouse Nestin Gene Contains A Centrasupporting

confidence: 73%

Different Transcription Factors Regulate nestin Gene Expression during P19 Cell Neural Differentiation and Central Nervous System Development

Jin

Liu

Bian

et al. 2009

Journal of Biological Chemistry

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Nestin is a molecular marker for neural progenitor cells. Rat and human nestin genes possess a central nervous system-specific enhancer within their second introns. However, the transcription factors that bind to the nestin enhancer have not been fully elucidated. Here, we show that the second intron of the mouse nestin gene is sufficient to drive reporter gene expression in the developing nervous system. The core sequence of this central nervous system-specific enhancer localizes to the 3 320-bp region. The cis-elements for Sox and POU family transcription factors and the hormone-responsive element are essential for nestin expression during embryonic carcinoma P19 cell neural differentiation and in the developing chick neural tube. Interestingly, different transcription factors bind to the nestin enhancer at different stages of P19 cell neural differentiation and central nervous system development. Sox2 and SF1 may mediate basal nestin expression in undifferentiated P19EC cells, whereas Sox2, Brn1, and Brn2 bind to the enhancer in P19 neural progenitor cells. Similarly, in vivo, Oct1 binds to the nestin enhancer in embryonic day 8.5 (E8.5) mouse embryos, and Oct1, Brn1, and Brn2 bind to this enhancer in E10.5 and E12.5 mouse embryos. Our studies therefore suggest a temporal coordination of transcription factors in determining nestin gene expression.

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Section: The Second Intron Of the Mouse Nestin Gene Contains A Centrasupporting

confidence: 73%

Different Transcription Factors Regulate nestin Gene Expression during P19 Cell Neural Differentiation and Central Nervous System Development

Jin

Liu

Bian

et al. 2009

Journal of Biological Chemistry

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“…In recent investigations, different functions of TTF1 have been discussed: in non-mucinous AC, TTF1 upregulates downstream surfactant genes [19], pointing to some inflammation regulating functions. TTF1 (also known as NKX2-1) is a transcription factor and prevents gastric differentiation in fetal lung.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary mucinous adenocarcinomas: architectural patterns in correlation with genetic changes, prognosis and survival

et al. 2015

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Of pulmonary adenocarcinomas, about 25-30 % of cases is of a mucinous type. Mucinous adenocarcinomas are regarded as more aggressive compared to their non-mucinous counterparts. Invasive mucinous adenocarcinoma, colloid, and enteric adenocarcinomas are variants within adenocarcinomas. We investigated 76 invasive mucinous adenocarcinomas, including colloid variants, for predominant and secondary patterns, their different form of mucin storage and release, expression of cytokeratin 7 and 20, TTF1 and CDX2, MUC1, 2, and 5AC proteins, p14 and p16 proteins, possible rearrangements for EML4ALK and ROS1, as well as KRAS mutational status, and correlated this with survival. For comparison, 259 non-mucinous adenocarcinomas were selected. Overall survival for invasive mucinous adenocarcinomas corrected for T and N stage was not different from their non-mucinous counterpart. Most were of an acinar pattern. Neither pattern, nor type of mucin storage and release, such as luminal, extracellular, or goblet cell type had any influence on survival. Of adenocarcinomas expressing CK20, all but one expressed TTF1 either strongly or at least focally, and 8 co-expressed CDX2 focally. Most mucinous adenocarcinomas expressed either MUC1 or MUC5AC proteins, but rarely MUC2, while a few cases co-expressed both or all three. Loss of p16 expression correlated with worse outcome. KRAS mutation was found in 56 % of mucinous adenocarcinomas. Mutational status was neither correlated with architectural pattern nor survival. Codon 12 mutations were most frequent, and one case presented with KRAS mutations in codon 12 and 61. Goblet cell variants of mucinous adenocarcinomas presented predominantly with codon 12 mutations, while all colloid variants had KRAS mutation. Two cases had EML4 and ALK1 rearranged; ROS1 rearrangement was not found. Mucinous adenocarcinomas behave similar to non-mucinous variants. TNM stage is the most important factor followed by p16 loss predicting overall survival.

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“…FOXA1 has been shown to repress NKX2-1 function by binding to its homeodomain and blocking NKX2-1 binding to DNA [as is the case for the surfactant protein C (SpC) promoter]. Importantly, for forebrain development, an early marker of proliferating neuroblasts, nestin, is a target of NKX2-1 both in vitro and in vivo (102,103). The difference between the two modes is that the former gene lacks a FOXA1-binding site, whereas the latter contains one.…”

Section: Nkx2-1 and Gsh2: Regulation Of Ventral Forebrain Developmentmentioning

confidence: 99%

“…In addition, SMAD3 (an effector of TGF‐β signaling) has been shown to block NKX2‐1 binding and thereby blunt its function (101). Importantly, for forebrain development, an early marker of proliferating neuroblasts, nestin, is a target of NKX2‐1 both in vitro and in vivo (102, 103).…”

Section: Nkx2‐1 and Gsh2: Regulation Of Ventral Forebrain Developmentmentioning

confidence: 99%

Homeobox genes in vertebrate forebrain development and disease

Wigle

Eisenstat

2008

Clinical Genetics

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Homeobox genes are an evolutionarily conserved class of transcription factors that are key regulators of developmental processes such as regional specification, patterning, migration and differentiation. In both mouse and humans, the developing forebrain is marked by distinct boundaries of homeobox gene expression at different developmental time points. These genes regulate the patterning of the forebrain along the dorsal/ventral and rostral/caudal axes and are also essential for the differentiation of specific neuronal subtypes. Inhibitory interneurons that arise from the ganglionic eminences and migrate tangentially to the neocortex and hippocampus are dramatically affected by mutations in several homeobox genes. In this review, we discuss the identification, expression patterns, loss- and/or gain-of-function models, and confirmed transcriptional targets for a set of homeobox genes required for the correct development of the forebrain in the mouse. In humans, mutations of homeobox genes expressed in the forebrain have been shown to result in mental retardation, epilepsy or movement disorders. The number of homeobox genes currently linked to human nervous system disease is surprisingly low, perhaps reflecting the essential functions of these genes throughout embryogenesis or the degree of functional redundancy during central nervous system development.

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TTF-1/NKX2.1 up-regulates the in vivo transcription of nestin

Cited by 11 publications

References 31 publications

Different Transcription Factors Regulate nestin Gene Expression during P19 Cell Neural Differentiation and Central Nervous System Development

Different Transcription Factors Regulate nestin Gene Expression during P19 Cell Neural Differentiation and Central Nervous System Development

Pulmonary mucinous adenocarcinomas: architectural patterns in correlation with genetic changes, prognosis and survival

Homeobox genes in vertebrate forebrain development and disease

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