Transcription Factor Foxq1 Controls Mucin Gene Expression and Granule Content in Mouse Stomach Surface Mucous Cells

Verzi, Michael P.; Khan, Abdul Hameed; Ito, Susumu; Shivdasani, Ramesh A.

doi:10.1053/j.gastro.2008.04.019

Cited by 51 publications

(52 citation statements)

References 42 publications

(61 reference statements)

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“…Nonetheless, many TFs are expressed and control genes in specific stomach cell types. Examples include FOXQ1, which is restricted to pit cells and required for the expression of the gastric mucin Muc5ac (Verzi et al, 2008) and the basic-helix-loop-helix TF MIST1, which enables proper chief cell differentiation (Ramsey et al, 2007;Tian et al, 2010). XBP1 controls the latter process by inducing Mist1 and expanding the rough endoplasmic reticulum (Huh et al, 2010a).…”

Section: Stomach Differentiation Epithelial (Mucosal) Differentiationmentioning

confidence: 99%

Stomach development, stem cells and disease

2016

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The stomach, an organ derived from foregut endoderm, secretes acid and enzymes and plays a key role in digestion. During development, mesenchymal-epithelial interactions drive stomach specification, patterning, differentiation and growth through selected signaling pathways and transcription factors. After birth, the gastric epithelium is maintained by the activity of stem cells. Developmental signals are aberrantly activated and stem cell functions are disrupted in gastric cancer and other disorders. Therefore, a better understanding of stomach development and stem cells can inform approaches to treating these conditions. This Review highlights the molecular mechanisms of stomach development and discusses recent findings regarding stomach stem cells and organoid cultures, and their roles in investigating disease mechanisms.

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Section: Stomach Differentiation Epithelial (Mucosal) Differentiationmentioning

confidence: 99%

Stomach development, stem cells and disease

2016

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“…Among the genes whose expression is increased in the ES cell-derived DE population, Foxq1 [50], CpM [51][52][53], Foxp4 [54,55], Pcdh1 [56], and Zmiz1 [57] were found to be expressed in the foregut, hindgut, or whole gut at E8.5. Parm1 [6], Tmem184 [58], HIPK-2 [59], Nptx2 [60,61], Tcf7l2 [62][63][64][65], C2Cd4b [66], Sox4 [67][68][69], and Kiss1r [70][71][72] were revealed for the first time to be expressed at this early stage of E8.5 and E14.5.…”

Section: Daf1/cd55 Foxq1 Nptx2 and Pga5mentioning

confidence: 99%

Profiling of Embryonic Stem Cell Differentiation

2014

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■ AbstractEmbryonic stem (ES) cells have been shown to recapitulate normal developmental stages. They are therefore a highly useful tool in the study of developmental biology. Profiling of ES cell-derived cells has yielded important information about the characteristics of differentiated cells, and allowed the identification of novel marker genes and pathways of differentiation. In this review, we focus on recent results from profiling studies of mouse embryos, human islets, and human ES cell-derived differentiated cells from several research groups. Global gene expression data from mouse embryos have been used to identify novel genes or pathways involved in the developmental process, and to search for transcription factors that regulate direct reprogramming. We introduce gene expression databases of human pancreas cells (Beta Cell Gene Atlas, EuroDia database), and summarize profiling studies of islet-or human ES cell-derived pancreatic cells, with a focus on gene expression, microRNAs, epigenetics, and protein expression. Then, we describe our gene expression profile analyses and our search for novel endoderm, or pancreatic, progenitor marker genes. We differentiated mouse ES cells into mesendoderm, definitive endoderm (DE), mesoderm, ectoderm, and Pdx1-expressing pancreatic lineages, and performed DNA microarray analyses. Genes specifically expressed in DE, and/or in Pdx1-expressing cells, were extracted and their expression patterns in normal embryonic development were studied by in situ hybridization. Out of 54 genes examined, 27 were expressed in the DE of E8.5 mouse embryos, and 15 genes were expressed in distinct domains in the pancreatic buds of E14.5 mouse embryos. Akr1c19, Aebp2, Pbxip1, and Creb3l1 were all novel, and none has been described as being expressed, either in the DE, or in the pancreas. By introducing the profiling results of ES cell-derived cells, the benefits of using ES cells to study early embryonic development will be discussed.

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“…FOXQ1 has a role in hair follicle development and FOXQ1 mutant mice have a silky shiny coat appearance [17]. Mice with FOXQ1 deficiency exhibit a lack of gastric acid secretion [19]. Accumulating evidence suggests that increased FOXQ1 expression is correlated with metastasis and poor prognosis for multiple human cancers, including breast cancer, colon cancer and lung cancer [20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

The hepatic FOXQ1 transcription factor regulates glucose metabolism in mice

et al. 2016

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Aim/hypothesis Hepatic forkhead box q1 (FOXQ1) expression levels are regulated by nutritional and pathophysiological status. In this study we investigated the role of FOXQ1 in the regulation of hepatic gluconeogenesis. Methods We used multiple mouse and cell models to study the role of FOXQ1 in regulating expression of gluconeogenic genes, and cellular and hepatic glucose production. Results Expression of hepatic FOXQ1 was regulated by fasting in normal mice and was dysregulated in diabetic mice. Overexpression of FOXQ1 in primary hepatocytes inhibited expression of gluconeogenic genes and decreased cellular glucose output. Hepatic FOXQ1 rescue in db/db and high-fat diet-induced obese mice markedly decreased blood glucose level and improved glucose intolerance. In contrast, wildtype C57 mice with hepatic FOXQ1 deficiency displayed increased blood glucose levels and impaired glucose tolerance. Interestingly, studies into molecular mechanisms indicated that FOXQ1 interacts with FOXO1, thereby blocking FOXO1 activity on hepatic gluconeogenesis, preventing it from directly binding to insulin response elements mapped in the promoter region of gluconeogenic genes. Conclusions/interpretation FOXQ1 is a novel factor involved in regulating hepatic gluconeogenesis, and the decreased FOXQ1 expression in liver may contribute to the development of type 2 diabetes.

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Transcription Factor Foxq1 Controls Mucin Gene Expression and Granule Content in Mouse Stomach Surface Mucous Cells

Cited by 51 publications

References 42 publications

Stomach development, stem cells and disease

Stomach development, stem cells and disease

Profiling of Embryonic Stem Cell Differentiation

The hepatic FOXQ1 transcription factor regulates glucose metabolism in mice

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