Thyroid hormone receptor/c-erbA: control of commitment and differentiation in the neuronal/chromaffin progenitor line PC12.

Múñoz, Alberto; Wrighton, Christopher J.; Seliger, Barbara; Bernal, Juan; Beug, H

doi:10.1083/jcb.121.2.423

Cited by 69 publications

(40 citation statements)

References 88 publications

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“…In line with the inability of the v-ErbA protein to bind T 3 , addition of hormone cannot release the repression of the NGF-induced neuronal differentiation. Besides this, T 3 does not affect the viability of PC12+v-erbA cells (80).…”

Section: Effects Of Trs In Neuronal Cellsmentioning

confidence: 99%

“…PC12 cells expressing the chicken TR-a gene (PC12+TRa-1) from an integrated Moloney murine leukemia-based retrovirus showed a very interesting phenotype: they were able to respond to the initial steps of the neuronal differentiation triggered by NGF with expression of a series of immediate early genes (c-jun, junB, junD, c-fos, fra-1, NGFI-A, NGFI-B) and formation of short processes (spikes), but were, however, blocked in later phases of differentiation with no elongation of neurites and the inhibition of the expression of the NGFinduced neuronal genes (transin, SCG10, neurofilament-68, NCAM, GAP43) (80). Thus, in the absence of hormone TR expression causes an inhibition of the NGFinduced neuronal differentiation pathway.…”

Section: Effects Of Trs In Neuronal Cellsmentioning

confidence: 99%

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Biological activities of thyroid hormone receptors

Múñoz

Bernal²

1997

European Journal of Endocrinology

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Section: Effects Of Trs In Neuronal Cellsmentioning

confidence: 99%

Section: Effects Of Trs In Neuronal Cellsmentioning

confidence: 99%

Biological activities of thyroid hormone receptors

Múñoz

Bernal²

1997

European Journal of Endocrinology

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“…However, to what extent C-to-S mutant PTPs can indeed be relied on to be specific and true dominant-negatives is as yet still unclear; hence, interpretation of the significance of this observation is probably premature. Assessment of mRNA levels by Northern blotting for the metalloprotease transin, a late marker for NGF-induced neuronal differentiation of PC12 cells (39,40), revealed that the EGF-induced neurite extension correlated fully with expression of this marker. EGF treatment lead to transin induction in cells expressing wt RPTP␣ or RPTP␣Y798F but not RPTP␣CCSS; moreover, this effect was stronger in RPTP␣Y798F than in wt RPTP␣-expressing cells (supplemental data included in the on-line version of manuscript).…”

Section: Rptp␣ Stimulates Egf-induced Neurite Outgrowth In a Mannermentioning

confidence: 99%

c-SRC Mediates Neurite Outgrowth through Recruitment of Crk to the Scaffolding Protein Sin/Efs without Altering the Kinetics of ERK Activation

Yang¹,

Alexandropoulos²,

Sap³

2002

Journal of Biological Chemistry

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SRC family kinases have been consistently and recurrently implicated in neurite extension events, yet the mechanism underlying their neuritogenic role has remained elusive. We report that epidermal growth factor (EGF) can be converted from a non-neuritogenic into a neuritogenic factor through moderate activation of endogenous SRC by receptor-protein-tyrosine phosphatase ␣ (a physiological SRC activator). We show that such a qualitative change in the response to EGF is not accompanied by changes in the extent or kinetics of ERK induction in response to this factor. Instead, the pathway involved relies on increased tyrosine phosphorylation of, and recruitment of Crk to, the SRC substrate Sin/Efs. The latter is a scaffolding protein structurally similar to the SRC substrate Cas, tyrosine phosphorylation of which is critical for migration in fibroblasts and epithelial cells. Expression of a dominant negative version of Sin interfered with receptor-protein-tyrosine phosphatase ␣/EGF-as well as fibroblast growth factorinduced neurite outgrowth. These observations uncouple neuritogenic signaling in PC12 cells from sustained activation of ERK kinases and for the first time identify an effector of SRC function in neurite extension.

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“…These brain regions (hippocampus, basal forebrain) have particularly high levels of thyroid hormone receptors during development and are sites where thyroid hormones regulate nerve growth factor (NGF) production (34)(35)(36). Thyroid hormones and NGF cooperate in the development of specific cholinergic systems in the central nervous system (37), and thyroid hormones could regulate neurotransmitter development through their action on NGF production in these specific regions. Hypothyroidism decreases choline acetyltransferase (ChAT) quantities in brain regions innervated by these neurons (32) because thyroid hormones serve as positive regulatory factors for the ChAT gene (38).…”

Section: Synaptogenesis and Myelinogenesismentioning

confidence: 99%

Thyroidal dysfunction and environmental chemicals--potential impact on brain development.

Porterfield

2000

Environ Health Perspect

137

129

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Certain polyhalogenated aromatic hydrocarbons such as polychlorinated biphenyls (PCBs) and dibenzo-p-dioxins (dioxins, 2,3,7,8-tetrachlorodibenzo-p-dioxin) have been shown to have neurotoxic effects and to alter thyroid function during critical periods of thyroid hormone-dependent brain development. This has led to the suggestion that some of the neurotoxic effects of these compounds could be mediated through the thyroid system. Thyroid hormones are essential for normal brain development during a critical period beginning in utero and extending through the first 2 years postpartum. They regulate neuronal proliferation, migration, and differentiation in discrete regions of the brain during definitive time periods. Even transient disruption of this normal pattern can impair brain development. Thyroid hormones are necessary for normal cytoskeletal assembly and stability and the cytoskeletal system is essential for migration and neuronal outgrowth. In addition, they regulate development of cholinergic and dopaminergic systems serving the cerebral cortex and hippocampus. Animals perinatally exposed to certain environmental organohalogens such as many of the PCBs and dioxins have abnormal thyroid function and neurologic impairment. Although there are both species and congener variabilities, most reports show exposure results in thyroid enlargement and reduced serum T4 levels with normal T3 levels. Initial research concentrated on studying the direct actions of xenobiotics on the thyroid; however, some of these compounds bear a structural resemblance to the natural thyroid hormones and have high affinity with thyroid hormone-binding proteins such as transthyretin. These compounds could act as agonists or antagonists for receptors of the thyroid/steroid/retinoic acid superfamily. These structurally similar organohalogens could act at multiple points to alter thyroid hormone action. The similarity of the neurologic impairment seen in thyroid disorders to that seen following PCB or dioxin exposure suggests that one mechanism of neurotoxicity of these compounds could involve interaction with the thyroid system.

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Thyroid hormone receptor/c-erbA: control of commitment and differentiation in the neuronal/chromaffin progenitor line PC12.

Cited by 69 publications

References 88 publications

Biological activities of thyroid hormone receptors

Biological activities of thyroid hormone receptors

c-SRC Mediates Neurite Outgrowth through Recruitment of Crk to the Scaffolding Protein Sin/Efs without Altering the Kinetics of ERK Activation

Thyroidal dysfunction and environmental chemicals--potential impact on brain development.

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