Identification of a Thyroid Hormone Response Element in the Mouse Krüppel-Like Factor 9 Gene to Explain Its Postnatal Expression in the Brain

Denver, Robert J.; Williamson, Keith

doi:10.1210/en.2009-0050

Cited by 83 publications

(73 citation statements)

References 38 publications

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“…Candidates for such a function are BTEB (Denver and Williamson, 2009), hairless (hr) (Potter et al, 2002), NeuroD (Chantoux and Francon, 2002), RORalpha (Koibuchi and Chin, 1998) and NGFI-A (Egr1) (Mellstrom et al, 1994). Moreover, recent approaches to identify further thyroid hormone regulated gene products in the brain using microarray analysis revealed additional T3 target genes (Poguet et al, 2003;Dong et al, 2005;Quignodon et al, 2007a;Diez et al, 2008).…”

Section: Molecular Targets Of Thyroid Receptorsmentioning

confidence: 99%

Thyroid hormone action during brain development: More questions than answers

Horn

Heuer

2010

Molecular and Cellular Endocrinology

176

109

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Section: Molecular Targets Of Thyroid Receptorsmentioning

confidence: 99%

Thyroid hormone action during brain development: More questions than answers

Horn

Heuer

2010

Molecular and Cellular Endocrinology

176

109

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“…There are three forms of such a pattern: direct repeat, inverted repeat, everted repeat and their reverse complement. Several methods have been used to predict NR binding sites (Bulyk, 2003;Cartharius et al, 2005;Denver and Williamson, 2009;Grau et al, 2006;Sandelin et al, 2004;Varga, 2010). One widely used method is NHR-Scan (Sandelin and Wasserman, 2005), a Hidden Markov Model (HMM) using 107 experimentally determined NRs to predict two half sites simultaneously.…”

Section: Introductionmentioning

confidence: 99%

NURBS: a database of experimental and predicted nuclear receptor binding sites of mouse

et al. 2012

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Summary: Nuclear receptors (NRs) are a class of transcription factors playing important roles in various biological processes. An NR often impacts numerous genes and different NRs share overlapped target networks. To fulfil the need for a database incorporating binding sites of different NRs at various conditions for easy comparison and visualization to improve our understanding of NR binding mechanisms, we have developed NURBS, a database for experimental and predicted nuclear receptor binding sites of mouse (NURBS). NURBS currently contains binding sites across the whole-mouse genome of 8 NRs identified in 40 chromatin immunoprecipitation with massively parallel DNA sequencing experiments. All datasets are processed using a widely used procedure and same statistical criteria to ensure the binding sites derived from different datasets are comparable. NURBS also provides predicted binding sites using NR-HMM, a Hidden Markov Model (HMM) model. Availability: The GBrowse-based user interface of NURBS is freely accessible at http://shark.abl.ku.edu/nurbs/. NR-HMM and all results can be downloaded for free at the website.

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“…We therefore investigated the involvement of high T 3 levels in the onset of the loss of regenerative capacity of postnatal PCs. Because Krüppel-like factor 9 (Klf9) is a transcriptional target of T 3 in some neuronal cell types (16,17) and is involved in the developmental loss of regenerative ability of retinal ganglion cells (5), we also examined whether T 3 acts on PCs by regulating Klf9 expression.…”

mentioning

confidence: 99%

Thyroid hormone triggers the developmental loss of axonal regenerative capacity via thyroid hormone receptor α1 and krüppel-like factor 9 in Purkinje cells

Avci

Lebrun

Wehrlé

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Neurons in the CNS of higher vertebrates lose their ability to regenerate their axons at a stage of development that coincides with peak circulating thyroid hormone (T 3 ) levels. Here, we examined whether this peak in T 3 is involved in the loss of axonal regenerative capacity in Purkinje cells (PCs). This event occurs at the end of the first postnatal week in mice. Using organotypic culture, we found that the loss of axon regenerative capacity was triggered prematurely by early exposure of mouse PCs to T 3 , whereas it was delayed in the absence of T 3 . Analysis of mutant mice showed that this effect was mainly mediated by the T 3 receptor α1. Using gain-and loss-of-function approaches, we also showed that Krüppel-like factor 9 was a key mediator of this effect of T 3 . These results indicate that the sudden physiological increase in T 3 during development is involved in the onset of the loss of axon regenerative capacity in PCs. This loss of regenerative capacity might be part of the general program triggered by T 3 throughout the body, which adapts the animal to its postnatal environment.axon regeneration | cerebellum | neural development | lentiviral vectors

show abstract

Identification of a Thyroid Hormone Response Element in the Mouse Krüppel-Like Factor 9 Gene to Explain Its Postnatal Expression in the Brain

Cited by 83 publications

References 38 publications

Thyroid hormone action during brain development: More questions than answers

Thyroid hormone action during brain development: More questions than answers

NURBS: a database of experimental and predicted nuclear receptor binding sites of mouse

Thyroid hormone triggers the developmental loss of axonal regenerative capacity via thyroid hormone receptor α1 and krüppel-like factor 9 in Purkinje cells

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