Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Germany  (48)
Collection
Keywords
  • 1
    Keywords: brain ; EXPRESSION ; Germany ; human ; GENE ; transcription ; MICE ; PATIENT ; ACTIVATION ; TRANSCRIPTION FACTOR ; MARKER ; PHOSPHORYLATION ; ASSOCIATION ; polymorphism ; CAMP ; ELEMENT-BINDING PROTEIN ; PATTERNS ; CYCLIC-AMP ; molecular ; PATTERN ; LIGHT ; analysis ; MEDICINE ; CIRCADIAN CLOCK ; MAJOR DEPRESSION ; SUPRACHIASMATIC-NUCLEI
    Abstract: Activation of the transcription factor CREB by Ser142 phosphorylation is implicated in synchronizing circadian rhythmicity, which is disturbed in many depressive patients. Hence, one could assume that emotional behaviour and neuroendocrinological markers would be altered in CREBS142A mice, in which serine 142 is replaced by alanine, preventing phosphorylation at this residue. Moreover, associations of CREB Ser142 and seasonal affective disorder (SAD) might be detectable by the analysis of single-nucleotide polymorphisms (SNPs) in the CREB gene close to the Ser142 residue in SAD patients. However, neither CREBS142A mice demonstrate features of depression, nor there is evidence for an association of SAD with the CREB genotypes. Nevertheless, in humans there is an association of a global seasonality score and circadian rhythmicity with the CREB genotypes in healthy control probands, but not SAD patients. This parallels the phenotype of CREBS142A mice, presenting alterations of circadian rhythm and light-induced entrainment. Thus it is reasonable to assume that CREB Ser142 represents a molecular switch in mice and men, which is responsible for the (dys)regulation of circadian rhythms. (C) 2007 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 17574346
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Keywords: brain ; RECEPTOR ; CELL ; Germany ; IN-VIVO ; MODEL ; MODELS ; VIVO ; SYSTEM ; TOOL ; METABOLISM ; MICE ; ACTIVATION ; RESPONSES ; MECHANISM ; mechanisms ; hippocampus ; MOUSE ; NERVOUS-SYSTEM ; DISRUPTION ; STRESS ; MUTATION ; DNA-BINDING ; MUTATIONS ; MOUSE MODEL ; glucocorticoid receptor ; DOMAINS ; DISSECTION ; review ; RE ; RESPONSIVENESS ; FOREBRAIN ; TECHNOLOGY ; LOSSES ; ENGLAND ; steroids ; STEROID-HORMONE RECEPTORS ; CRE RECOMBINASE ACTIVITY ; cortisol/corticosterone ; HPA axis
    Abstract: In the brain, glucocorticoids exert functions in neurogenesis, synaptic plasticity and behavioural responses, as well as in the control of hypothalamic-pituitary-adrenal axis activity. The generation of mice harbouring germline mutations that result either in loss or in gain of glucocorticoid receptor function provided a useful tool for understanding the role of glucocorticoids in the brain in vivo. The improvement of genomic technologies additionally allowed the establishment of mouse models with function-selective point mutations of the receptor as well as the generation of mice harbouring spatially and/or temporally restricted loss of glucocorticoid receptor, specifically within the brain. These models will provide the opportunity to better understand the mechanisms involved in glucocorticoid signalling within the nervous system
    Type of Publication: Journal article published
    PubMed ID: 18513206
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: APOPTOSIS ; CELLS ; GROWTH ; proliferation ; SURVIVAL ; CELL ; Germany ; INHIBITION ; SYSTEM ; DEATH ; GENE ; GENES ; RNA ; transcription ; MICE ; ACTIVATION ; TRANSCRIPTION FACTOR ; INDUCTION ; hippocampus ; NERVOUS-SYSTEM ; TRANSCRIPTIONAL ACTIVITY ; DISRUPTION ; CELL-DEATH ; STRESS ; inactivation ; p53 ; STRATEGIES ; INTERACTS ; HEALTHY ; molecular ; ADULT ; RE ; FACTOR TIF-IA ; NEURONS ; ABLATION ; LEVEL ; cell death ; nucleolus ; RNA polymerase I ; progenitor ; INDUCE ; USA ; LOSSES ; neurodegeneration ; PROGENITORS ; DEGENERATION ; NOV ; response ; synthesis ; POLYMERASE ; STATE ; RNA-POLYMERASE ; neural progenitors ; rRNA transcription ; TRANSCRIPTION ACTIVITY
    Abstract: Transcription of rRNA genes is essential for maintaining nucleolar integrity, a hallmark for the healthy state and proliferation rate of a cell. Inhibition of rRNA synthesis leads to disintegration of the nucleolus, elevated levels of p53, and induction of cell suicide, identifying the nucleolus as a critical stress sensor. Whether deregulation of rRNA synthesis is causally involved in neurodegeneration by promoting cell death and/or by inhibiting cellular growth has however not been addressed. The transcription factor TIF-IA plays a central role in mammalian rRNA synthesis, regulating the transcriptional activity of RNA polymerase I. To investigate the consequences of nucleolar perturbation in the nervous system, we have chosen to specifically ablate the gene encoding the transcription factor TIF-IA in two different contexts: neural progenitors and hippocampal neurons. Here, we show that ablation of TIF-IA leads to impaired nucleolar activity and results in increased levels of the proapoptotic transcription factor p53 in both neural progenitors and hippocampal neurons but induces rapid apoptosis only in neural progenitors. Nondividing cells of the adult hippocampus are more refractory to loss of rRNA transcription and face a protracted degeneration. Our study provides an unexploited strategy to initiate neurodegeneration based on perturbation of nucleolar function and underscores a novel perspective to study the cellular and molecular changes involved in the neurodegenerative processes
    Type of Publication: Journal article published
    PubMed ID: 19036968
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Keywords: RECEPTOR ; EXPRESSION ; IN-VITRO ; PROTECTION ; Germany ; IN-VIVO ; VITRO ; VIVO ; SYSTEM ; SYSTEMS ; NEW-YORK ; MICE ; MECHANISM ; mechanisms ; TYPE-1 ; ACID ; NERVOUS-SYSTEM ; DAMAGE ; CENTRAL-NERVOUS-SYSTEM ; MUTANT MICE ; max ; ACUTE NEURONAL INJURY ; ANANDAMIDE ; ENDOCANNABINOIDS ; GLUTAMATE ; N-ACYLETHANOLAMINE PHOSPHOLIPIDS ; NEUROPROTECTION ; RAT-BRAIN ; SEIZURE
    Abstract: Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice, the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protective mechanisms could not be triggered in mutant mice. The endogenous cannabinoid system thus provides on-demand protection against acute excitotoxicity in central nervous system neurons
    Type of Publication: Journal article published
    PubMed ID: 14526074
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Keywords: brain ; RECEPTOR ; EXPRESSION ; GROWTH ; evaluation ; Germany ; IN-VIVO ; MODEL ; MODELS ; PATHWAY ; PATHWAYS ; VIVO ; SUPPORT ; SYSTEM ; DISTINCT ; GENE ; GENE-EXPRESSION ; GENES ; PROTEINS ; transcription ; MICE ; ACTIVATION ; RESPONSES ; DNA ; TRANSCRIPTION FACTOR ; hepatocytes ; INTERVENTION ; MR ; BINDING ; MEMORY ; TARGET ; MOUSE ; TRANSCRIPTION FACTORS ; hormone ; IDENTIFICATION ; gene expression ; TRANSCRIPTIONAL ACTIVITY ; DISRUPTION ; MUTATION ; DISPLAY ; DNA-BINDING ; MUTATIONS ; US ; MOUSE MODEL ; glucocorticoid receptor ; BODY ; side effects ; RECEPTORS ; INSIGHTS ; CRE RECOMBINASE ; GLUCOCORTICOID-RECEPTOR ; REPRESSION ; DIMERIZATION ; immunosuppression ; DISSECTION ; steroid ; signaling ; targeting ; BODIES ; molecular ; RE ; INTERFERENCE ; RESOURCE ; regulation ; gene targeting ; GENE-REGULATION ; GENE-TRANSCRIPTION ; MOUSE MODELS ; TARGET GENE ; corticosteroid ; gene regulation ; mineralocorticoid receptor ; SI
    Abstract: Functional genomic technologies, including artificial chromosome-based transgenesis and conditional gene targeting, allowed us to generate mouse models harboring genes with loss-of-function mutations, gain-of-function mutations, spatially and/or temporally restricted mutations, tissue-specific mutations, and function-selective mutations. This kind of "allelic series" for corticosteroid receptors in mouse models provides a very useful resource for the molecular understanding of corticosteroid function in vivo. These models will also support the identification of steroid receptor target genes in order to define a steroid signaling cascade in molecular terms. They provide opportunities for the identification of compounds that regulate steroid receptors in a tissue-specific and function-selective manner. For example, selective glucocorticoid receptor modulators preventing receptor dimerization and DNA binding can be expected to reduce osteoporotic and/or diabetogenic side effects, but to display partial or full anti-inflammatory potential. Thus, these mouse models will help to evaluate distinct steroid receptor functions for therapeutic intervention.
    Type of Publication: Journal article published
    PubMed ID: 15241729
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Keywords: brain ; CELLS ; EXPRESSION ; IN-VITRO ; Germany ; DENSITY ; SYSTEM ; GENE ; GENE-EXPRESSION ; transcription ; TRANSCRIPTION FACTOR ; PHOSPHORYLATION ; DELETION ; MOUSE ; NERVOUS-SYSTEM ; LIM-KINASE ; CELL-MIGRATION ; ACTIN CYTOSKELETON ; TARGET GENE ; TERNARY COMPLEX ; ACTIN DYNAMICS ; C-FOS PROMOTER ; cell migration ; cofilin ; FOREBRAIN ; SERUM RESPONSE FACTOR ; SRF ; TARGET GENES
    Abstract: The central nervous system is fundamentally dependent on guided cell migration, both during development and in adulthood. We report an absolute requirement of the transcription factor serum response factor (SRF) for neuronal migration in the mouse forebrain. Conditional, late-prenatal deletion of Srf causes neurons to accumulate ectopically at the subventricular zone (SVZ), a prime neurogenic region in the brain. SRF-deficient cells of the SVZ exhibit impaired tangential chain migration along the rostral migratory stream into the olfactory bulb. SVZ explants display retarded chain migration in vitro. Regarding target genes, SRF deficiency impairs expression of the beta-actin and gelsolin genes, accompanied by reduced cytoskeletal actin fiber density. At the posttranslational level, cofilin, a key regulator of actin dynamics, displays dramatically elevated inhibitory phosphorylation at Ser-3. Our studies indicate that SRIF-controlled gene expression directs both the structure and dynamics of the actin microfilament, thereby determining cell-autonomous neuronal migration
    Type of Publication: Journal article published
    PubMed ID: 15837932
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; Germany ; PATHWAY ; SYSTEM ; SITE ; SITES ; GENE ; GENES ; transcription ; MICE ; TRANSCRIPTION FACTOR ; RAT ; MOLECULE ; NERVOUS-SYSTEM ; TRANSCRIPTION FACTORS ; MUTATION ; DERIVATIVES ; MUTATIONS ; Jun ; glucocorticoid receptor ; GLUCOCORTICOID-RECEPTOR ; targeted ; MICE LACKING ; REQUIREMENT ; NEURONS ; GLAND ; development ; progenitor ; signalling ; GLUCOCORTICOIDS ; ACHAETE-SCUTE HOMOLOG-1 ; adrenal chromaffin cells ; GANGLION-CELLS ; GRANULE-CONTAINING CELLS ; neural crest ; NEURAL CREST DERIVATIVES ; sympathetic nervous system
    Abstract: This article summarizes some of the recent progress in understanding the development of chromaffin cells. These cells are derivatives of the neural crest and are intimately associated with the sympathetic nervous system. Although a common sympathoadrenal (SA) progenitor cell for chromaffin cells and sympathetic neurons has been postulated, there is evidence to suggest that chromaffin progenitors are already distinct, at least in part, from neuronal SA progenitors prior to invading the adrenal gland. The concept of an essential role of glucocorticoid signalling for chromaffin cell development has been shaken by the observation that chromaffin cells in mice lacking the glucocorticoid receptor develop largely normal. Distinct developmental requirements of chromaffin cells and sympathetic neurons must also be assumed based on the analyses of mice carrying targeted mutations of the genes for two transcription factors, MASH1 and Phox2B. Both genes are expressed by SA progenitors, but are distinctly required for the development of chromaffin cells and sympathetic neurons. There is an ongoing search for molecules selectively operating at the sites, where chromaffin cells develop. Such molecules may be candidates for triggering the distinct developmental pathway of chromaffin cells, as opposed to sympathetic neurons
    Type of Publication: Journal article published
    PubMed ID: 16187226
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Keywords: EXPRESSION ; SURVIVAL ; Germany ; PATHWAY ; PATHWAYS ; GENERATION ; SYSTEM ; DISEASE ; DISEASES ; GENE ; PROTEIN ; transcription ; MICE ; ACTIVATION ; TRANSCRIPTION FACTOR ; BINDING ; PHOSPHORYLATION ; CREB ; ELEMENT-BINDING PROTEIN ; TRANSCRIPTION FACTORS ; DISRUPTION ; MUTATION ; LINE ; inactivation ; SIGNALING PATHWAY ; SIGNALING PATHWAYS ; PHENOTYPE ; MUTANT MICE ; CYCLIC-AMP ; BINDING PROTEIN ; signaling ; MICE LACKING ; function ; LOSSES ; neuron ; CAMP RESPONSE ELEMENT ; dopaminergic neurons ; MESENCEPHALIC DOPAMINERGIC-NEURONS ; MIDBRAIN ; TRANSPORTER MESSENGER-RNA
    Abstract: cAMP response element binding protein (CREB) and the related factors CREM (cAMP response element modulator) and ATF1 (activation transcription factor 1) are bZIP-domain-containing transcription factors activated through cAMP and other signaling pathways. The disruption of CREB function in developing and mature neurons affects their development and survival when associated with loss of CREM. Since dopaminergic (DA) neurons are affected in several neurological diseases, we generated CREB conditional mutants in DA neurons by using a newly generated transgenic Cre line targeting the dopaminergic system (DATCre). Here we report the generation and analysis of mutant mice lacking CREB in DA neurons (CREBDATCre mutants). During adulthood, lack of CREB leads to a partial loss of DA neurons. Since CREM is upregulated in absence of CREB, we have introduced this mutation in a CREM-/- genetic background to assess a compensatory role of CREM. Additional inactivation of CREM does not lead to a more severe phenotype
    Type of Publication: Journal article published
    PubMed ID: 16981198
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    Keywords: RECEPTOR ; CELL ; Germany ; PATHWAY ; MICE ; MECHANISM ; mechanisms ; ALPHA ; virus ; MOUSE ; NERVOUS-SYSTEM ; hormone ; LINE ; REGION ; REGIONS ; BETA ; MUTANT MICE ; RAT-BRAIN ; ESTROGEN-RECEPTOR ; RE ; DEPENDENT PROTEIN-KINASE ; ESTROGEN ; estrogen receptor ; PSEUDORABIES VIRUS ; neuron ; FEMALE RAT ; LHRH NEURONS ; LUTEINIZING-HORMONE ; PREOPTIC AREA ; SURGE
    Abstract: The mechanisms through which estrogen regulates gonadotropin-releasing hormone (GnRH) neurons to control mammalian ovulation are unknown. We found that estrogen positive feedback to generate the preovulatory gonadotropin surge was normal in estrogen receptor beta knockout (ER beta) mutant mice, but absent in ER alpha mutant mice. An ER alpha-selective compound was sufficient to generate positive feedback in wild-type mice. As GnRH neurons do not express ER alpha, estrogen positive feedback upon GnRH neurons must be indirect in nature. To establish the cell type responsible, we generated a neuron-specific ERa mutant mouse line. These mice failed to exhibit estrogen positive feedback, demonstrating that neurons expressing ER alpha are critical. We then used a GnRH neuron-specific Pseudorabies virus (PRV) tracing approach to show that the ER alpha-expressing neurons innervating GnRH neurons are located within rostral periventricular regions of the hypothalamus. These studies demonstrate that ovulation is driven by estrogen actions upon ER alpha-expressing neuronal afferents to GnRH neurons
    Type of Publication: Journal article published
    PubMed ID: 17046690
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    Keywords: brain ; RECEPTOR ; Germany ; IN-VIVO ; DIFFERENTIATION ; TISSUE ; MICE ; TISSUES ; TRANSGENIC MICE ; signaling ; CYTOKINE ; RE ; GLAND ; VIP ; DEVELOPMENTAL EXPRESSION ; neuron ; cholinergic ; CILIARY NEUROTROPHIC FACTOR ; IL6/IL-6 ; LEUKEMIA INHIBITORY FACTOR ; PEPTIDERGIC PROPERTIES ; PLASTICITY INVIVO ; RAT SWEAT GLANDS ; RECEPTOR-ALPHA-COMPONENT ; SECRETORY RESPONSIVENESS ; sympathetic ; VAChT ; VESICULAR ACETYLCHOLINE TRANSPORTER
    Abstract: Sympathetic neurons are generated through a succession of differentiation steps that initially lead to noradrenergic neurons innervating different peripheral target tissues. Specific targets, like sweat glands in rodent footpads, induce a change from noradrenergic to cholinergic transmitter phenotype. Here, we show that cytokines acting through the gp130 receptor are present in sweat glands. Selective elimination of the gp130 receptor in sympathetic neurons prevents the acquisition of cholinergic and peptidergic features (VAChT, ChT1, VIP) without affecting other properties of sweat gland innervation. The vast majority of cholinergic neurons in the stellate ganglion, generated postnatally, are absent in gp130-deficient mice. These results demonstrate an essential role of gp130-signaling in the target-dependent specification of the cholinergic neurotransmitter phenotype
    Type of Publication: Journal article published
    PubMed ID: 16319110
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...