PTF1 Is an Organ-Specific and Notch-Independent Basic Helix-Loop-Helix Complex Containing the Mammalian Suppressor of Hairless (RBP-J) or Its Paralogue, RBP-L

Beres, Thomas M.; Masui, Toshihiko; Swift, Galvin H.; Shi, Ling; Henke, R. Michael; MacDonald, Raymond J.

doi:10.1128/mcb.26.1.117-130.2006

Cited by 195 publications

(311 citation statements)

References 44 publications

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“…Therefore, Mist1 is necessary for proper cell polarization and maintenance of acinar identity. RBPL is essential for the high transcriptional activity of the PTF1 complex independently of Notch signaling (22). Interestingly, RBPL is expressed in the developing pancreas tips at E14.5 (23), when exocrine precursors expand and differentiate, confirming a role in acinar differentiation during the secondary transition (24).…”

Section: Introductionmentioning

confidence: 85%

Murine Embryonic Stem Cell–Derived Pancreatic Acinar Cells Recapitulate Features of Early Pancreatic Differentiation

et al. 2008

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Background & Aims-Acinar cells constitute 90% of the pancreas epithelium, are polarized, and secrete digestive enzymes. These cells play a crucial role in pancreatitis and pancreatic cancer. However, there are no models to study normal acinar cell differentiation in vitro. The aim of this work was to generate and characterize purified populations of pancreatic acinar cells from embryonic stem cells (ES).

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Section: Introductionmentioning

confidence: 85%

Murine Embryonic Stem Cell–Derived Pancreatic Acinar Cells Recapitulate Features of Early Pancreatic Differentiation

et al. 2008

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“…The trimeric Pancreas Transcription Factor 1 complex (PTF1) was first identified as an acinar enzyme gene activator (Rose et al, 1994;Krapp et al, 1996) and comprises a tissuespecific bHLH protein, Ptf1a; an ubiquitous bHLH protein, E2A or HEB (formerly known as p75, which provides a constitutive nuclear import function for the PTF1 protein complex) (Rose et al, 1994, Krapp et al, 1996, Sommer et al, 1991; and the distinct mammalian Suppressor of Hairless (RBP-J) protein, or the RBP-JL paralog (Obata et al, 2001;Beres et al, 2006). Ptf1a is expressed as early as E9.5 in most cells of the nascent pancreatic buds, and is essential for pancreas organogenesis in mouse and human (Kawaguchi et al, 2002;Krapp et al, 1998;Sellick et al, 2004).…”

Section: Ptf1amentioning

confidence: 99%

“…Since RBP-J and RBP-JL differ in transcriptional activity, the switch in TC-box-binding factor may cause an alteration in Pdx1 expression (and perhaps other genes that guide progenitor-to-differentiated cell transitions), from high levels in early MPC to the lower levels needed for acinar differentiation (Beres et al, 2006;Wiebe et al, 2007;Miyatsuka et al, 2007). These studies, together with the evidence above from frog embryo misexpression studies, point out the importance of positive cross-regulation between Ptf1a and Pdx1 in creating or maintaining the pancreatic ''MPC metastable phase'' as a priming phase for pancreatic progenitors in early stage organogenesis.…”

Section: Developmental Dynamicsmentioning

confidence: 99%

Pancreas organogenesis: From bud to plexus to gland

Pan

Wright

2011

Developmental Dynamics

528

594

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Pancreas oganogenesis comprises a coordinated and highly complex interplay of signaling events and transcriptional networks that guide a step-wise process of organ development from early bud specification all the way to the final mature organ state. Extensive research on pancreas development over the last few years, largely driven by a translational potential for pancreatic diseases (diabetes, pancreatic cancer, and so on), is markedly advancing our knowledge of these processes. It is a tenable goal that we will one day have a clear, complete picture of the transcriptional and signaling codes that control the entire organogenetic process, allowing us to apply this knowledge in a therapeutic context, by generating replacement cells in vitro, or perhaps one day to the whole organ in vivo. This review summarizes findings in the past 5 years that we feel are amongst the most significant in contributing to the deeper understanding of pancreas development. Rather than try to cover all aspects comprehensively, we have chosen to highlight interesting new concepts, and to discuss provocatively some of the more controversial findings or proposals. At the end of the review, we include a perspective section on how the whole pancreas differentiation process might be able to be unwound in a regulated fashion, or redirected, and suggest linkages to the possible reprogramming of other pancreatic cell-types in vivo, and to the optimization of the forward-directed-differentiation of human embryonic stem cells (hESC), or induced pluripotential cells (iPSC), towards mature b-cells. Developmental Dynamics 240:530-565,

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“…Although RBP-L did not interact with any Notch protein, it was shown to cooperate with EBNA2 in transcriptional activation. RBP-L has been also found in complex with PTF1, which has been proposed to play a role in pancreas development [66]. The physiological role and possible redundancy of the two RBP factors is still unknown.…”

Section: Epigenetic Regulation Of Notch Target Genesmentioning

confidence: 99%

“…Vol. 66,2009 Review Article 1639 poietic progenitors on these stromal Notch-ligand expressing cells [139]. Notch signaling also potentially plays a role in the development of gamma/delta T-cells and natural killer cell development, reviewed in [107,140].…”

Section: T-cell Developmentmentioning

confidence: 99%

The Notch signaling pathway: Transcriptional regulation at Notch target genes

Borggrefe

Oswald

2009

Cell. Mol. Life Sci.

584

499

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. The Notch gene encodes a transmembrane receptor that gave the name to the evolutionary highly conserved Notch signaling cascade. It plays a pivotal role in the regulation of many fundamental cellular processes such as proliferation, stem cell maintenance and differentiation during embryonic and adult development. After specific ligand binding, the intracellular part of the Notch receptor is cleaved off and translocates to the nucleus, where it binds to the transcription factor RBP-J. In the absence of activated Notch, RBP-J represses Notch target genes by recruiting a corepressor complex. Here, we review Notch signaling with a focus on gene regulatory events at Notch target genes. This is of utmost importance to understand Notch signaling since certain RBP-J associated cofactors and particular epigenetic marks determine the specificity of Notch target gene expression in different cell types. We subsequently summarize the current knowledge about Notch target genes and the physiological significance of Notch signaling in development and cancer.

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PTF1 Is an Organ-Specific and Notch-Independent Basic Helix-Loop-Helix Complex Containing the Mammalian Suppressor of Hairless (RBP-J) or Its Paralogue, RBP-L

Cited by 195 publications

References 44 publications

Murine Embryonic Stem Cell–Derived Pancreatic Acinar Cells Recapitulate Features of Early Pancreatic Differentiation

Murine Embryonic Stem Cell–Derived Pancreatic Acinar Cells Recapitulate Features of Early Pancreatic Differentiation

Pancreas organogenesis: From bud to plexus to gland

The Notch signaling pathway: Transcriptional regulation at Notch target genes

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