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Results highlight the possibility that Ptf1a may act as an important transcription factor for enteric neuron development.
In ptf1a haploinsufficiency, more ptf1a-lineage-labeled cells are traced into the pancreatic Notch-responsive cell and endocrine compartments. More reduction of ptf1a gene dosage converts pancreatic progenitor cells to non-pancreatic cell fates.
Autoregulation of ptf1a is absolutely required for exocrine pancreas formation.
Postembryonic antagonism of Ptf1a, a master regulator of pancreatic development and acinar cell fate specification, induced expression of endocrine genes including insulin in the exocrine compartment. Induced insulin+ cells are derived from acinar cells.
The timing of Ptf1a expression suggests that it is involved in the very early stages or steps in the differentiation of amacrine cells, which can be seen to rapidly diversify into a large number of subtypes.
mapping, analysis of embryonic expression and role in pancreas development
Ptf1 function is inhibited by notch
We propose that low levels of Ptf1a promote endocrine fate, whereas high levels repress endocrine fate and promote exocrine fate.
Exocrine differentiation and proliferation factor (exdpf) is a direct target gene of pancreas-specific transcription factor 1a (Ptf1a).
Our results demonstrate that Prdm13, downstream of Ptf1a, acts as an important regulator of glycinergic amacrine subtype specification in the Xenopus retina. We also reveal that Prdm13 regulates ptf1a expression through a negative feedback loop.
Xenopus Ptf1a is essential for the initial specification of both endocrine and exocrine cells during normal pancreas development.
Ptf1a overexpression leads to an increased ratio of GABAergic subtypes among the whole amacrine and horizontal cell population, highlighting its instructive capacity to promote this specific subtype of inhibitory neurons
analysis of the gene regulatory network activated by Ptf1a in early pancreas development;results revealed that Ptf1a regulates genes with a wide variety of functions, providing insight into the complexity of the regulatory network required for pancreas specification
non-neural progenitor transcription factor Ptf1a alone is sufficient to directly reprogram mouse and human fibroblasts into self-renewable induced neural stem cells capable of differentiating into functional neurons, astrocytes and oligodendrocytes, and improving cognitive dysfunction of Alzheimer's disease mouse models when transplanted
Study describes the wide range of gene control by PTF1A that maintains the specific characteristics of pancreatic acinar cell identity and differentiation. PTF1A controls the pancreatic acinar transcription program by direct action at a thousand genes and in collaboration with other less cell type-restricted factors to ensure acinar cell homeostasis and to suppress other cell-type-specific programs.
Data show isolated Pancreatic Aplasia Due to a Hypomorphic PTF1A Mutation
The results of this study suggested Ptf1a-dependent cell-fate misspecification as a novel mechanism of human brainstem pathology.
PTF1A enhancer mutations have been shown to cause neonatal diabetes associated with pancreatic agenesis
Loss of Ptf1a alone is sufficient to induce acinar-to-ductal metaplasia, potentiate inflammation, and induce a KRAS-permissive, pancreatic ductal adenocarcinoma-like gene expression profile.
The results of the present study do not support the hypothesis that high penetrant mutations in these regions of PTF1A are involved in the development of human VATER/VACTERL association or NTDs
ata indicate that E3 ubiquitin ligase thyroid hormone receptor-interacting protein 12 (TRIP12) promotes proteasomal degradation of pancreas transcription factor 1a (PTF1a)and regulates PTF1a activities.
Recessive mutations in a distal PTF1A enhancer cause isolated pancreatic agenesis.
ICAT is a novel Ptf1a interactor that regulates pancreatic acinar differentiation and displays altered expression.
ptf1a functions as a "pancreatic determiner".
P48 interacts with the RBP-L and RBP-J subunits primarily through two short conserved tryptophan-containing motifs, similar to the motif of the Notch intracellular domain (NotchIC) that interacts with RBP-J.
Controls the fate, survival, differentiation, and migration of climbing fiber neurons during their development in the transgenic murine inferior olivary nucleus.
A critical and selective role of p/CAF in PTF1-dependent gene activation during acinar differentiation.
Here we report a new case of cerebellar agenesis and neonatal diabetes mellitus whose parents are PTF1A mutation carriers.
Two separable genomic regions code for initiation and positive feedback of Ptf1a transgene expression in the developing nervous system.
We crossed Ptf1a(Cre/+) ;Kras(G12D/+) mice with JNK1(-/-) mice to generate Ptf1a(Cre/+) ;Kras(G12D/+) ;JNK1(-/-) (Kras;JNK1(-/-) ) mice. Tumor weight was significantly lower in Kras;JNK1(-/-) mice than in Kras;JNK1(+/-) mice, whereas histopathological features were similar.we concluded that inhibition of activated JNK in pancreatic tumor stroma could be a potential therapeutic target to increase Ccl20 secretion
Ptf1a is regulated by active and repressive inputs integrated through multiple sequence elements within a highly conserved sequence downstream of the Ptf1a gene.
the Tfap2a and Tfap2b transcription factors were identified as two major downstream effectors of Ptf1a.
This study demonstrated that the transcription factor Ptf1a is capable of cell autonomously redirecting cortical pyramidal cell identity toward an inhibitory peptidergic fate.
We provide strong evidence for spatiotemporally context-dependent activity of Ptf1a as a potent gain-of-function trigger of pro-pancreatic commitment.
Data suggest the role of pancreas-specific transcription factor 1a (PTF1a) in pancreas development in directing differentiation of embryonic stem cells (ESCs) to endocrine cells.
GABAergic inducing activity of Ascl1 requires the direct transcriptional regulation of Ptf1a.
Ascl1 and Ptf1a directly regulate distinct homeodomain transcription factors that specify excitatory or inhibitory neuronal fates.
These data identify Ptf1a as the first gene involved in the segregation of the cerebellum from the more ventral brainstem.
The results of this study suggested that Ptf1a specify spatial identities of cerebellar neuron progenitors in the neuroepithelium, leading to appropriate production of GABAergic and glutamatergic neurons, respectively.
The results support a model whereby Ptf1a directs distinct gene expression programs that are established by the interplay of chromatin accessibility, collaborating transcription factors, and the DNA motifs within tissue-specific regulatory enhancers.
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Ptf1a-deficient mice lack all inhibitory interneurons in the dorsal horn.
we demonstrated that misexpression of Ptf1a, but not of Gm13344 or Gm13336, in the notochord, hindgut, cloaca, and mesonephros was sufficient to replicate the Sd phenotype
We show that Ptf1a expression is significantly upregulated in Sd mutant embryos.
The Sd heterozygote phenotype was not ameliorated by Ptf1a haploinsufficiency, further suggesting that the developmental defects result from ectopic expression of Ptf1a.
binding of Rbms3 to the 3'UTR of Ptf1a regulates the production of the Ptf1a protein
Tlx1/3 and Ptf1a, the key transcription factors for fate determination of glutamatergic and GABAergic neurons in the dorsal spinal cord
Mnx1, a gene that is absolutely required in pancreas progenitors, is a major direct target of Ptf1a and is regulated by a distant enhancer element.
This gene encodes a protein that is a component of the pancreas transcription factor 1 complex (PTF1) and is known to have a role in mammalian pancreatic development. The protein plays a role in determining whether cells allocated to the pancreatic buds continue towards pancreatic organogenesis or revert back to duodenal fates. The protein is thought to be involved in the maintenance of exocrine pancreas-specific gene expression including elastase 1 and amylase. Mutations in this gene cause cerebellar agenesis and loss of expression is seen in ductal type pancreas cancers.
pancreas specific transcription factor, 1a
, bHLH transcription factor p48
, pancreas transcription factor 1 subunit alpha
, pancreas-specific transcription factor 1a
, Pancreas-specific transcription factor 1a
, transcription factor Ptf1a/p48
, class A basic helix-loop-helix protein 29
, class II bHLH protein PTF1A
, exocrine pancreas-specific transcription factor p48
, p48 DNA-binding subunit of transcription factor PTF1
, pancreas transcription factor1 p48 subunit