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Results for “Expression divergence”

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PubMed1990

Induction of the nag regulon of Escherichia coli by N-acetylglucosamine and glucosamine: role of the cyclic AMP-catabolite activator protein complex in expression of the regulon.

The divergent nag regulon located at 15.5 min on the Escherichia coli map encodes genes necessary for growth on N-acetylglucosamine and glucosamine. Full induction of the regulon requires both the presence of N-acetylglucosamine and a functional cyclic AMP (cAMP)-catabolite activator protein (CAP) complex. Glucosamine produces a lower level of induction of the regulon. A nearly symmetric consensus CAP-binding site is located in the intergenic region between nagE (encoding EIINag) and nagB (encoding glucosamine-6-phosphate deaminase). Expression of both nagE and nagB genes is stimulated by cAMP-CAP, but the effect is more pronounced for nagE. In fact, very little expression of nagE is observed in the absence of cAMP-CAP, whereas 50% maximum expression of nagB is observed with N-acetylglucosamine in the absence of cAMP-CAP. Two mRNA 5' ends separated by about 100 nucleotides were located before nagB, and both seem to be similarly subject to N-acetylglucosamine induction and cAMP-CAP stimulation. To induce the regulon, N-acetylglucosamine or glucosamine must enter the cell, but the particular transport mechanism used is not important.

Acetylglucosamine↗
PubMed2005

Divergent effects of estrogen and nicotine on Rho-kinase expression in human coronary vascular smooth muscle cells.

Recent studies have demonstrated that up-regulated Rho-kinase plays an important role in the pathogenesis of coronary arteriosclerosis and vasospasm. We have shown that inflammatory stimuli, such as angiotensin II and interleukin-1beta, up-regulate Rho-kinase expression and activity in human coronary vascular smooth muscle cells, for which intracellular signal transduction mediated by protein kinase C and NF-kappaB is involved. Here, we show that estrogen down-regulates while nicotine up-regulates Rho-kinase and that nicotine counteracts the inhibitory effect of estrogen on angiotensin II-induced Rho-kinase expression. Furthermore, we demonstrated that the intracellular signal transduction of the inhibitory effect of estrogen is mediated by an estrogen receptor. These results demonstrate that inflammatory stimuli up-regulate Rho-kinase, for which estrogen (mediated by an estrogen receptor) and nicotine exert divergent inhibitory and stimulatory effects on the Rho-kinase expression, respectively, and may explain in part why the incidence of arteriosclerotic and vasospastic disorders is increased in postmenopausal women and smokers.

Angiotensin II↗
PubMedDate not supplied

Mycoplasma gallisepticum--induced alterations in cytokine genes in chicken cells and embryos.

Mycoplasma gallisepticum (MG) was used to infect the MSB-1 cells, the HD-11 cells, and chicken embryos. The RNA from these cells and the embryonic spleen cells were extracted and assayed for the expression of cytokine genes using reverse transcription-polymerase chain reaction. The results showed that MG infection suppressed the expression of the IL-8 gene in the MSB-1 cells and enhanced the expression of the IL-8 and IL-6 genes in the HD-11 cells; a slightly increased expression of macrophage inflammatory protein-1beta (MIP-1beta) in MG-infected spleen cells was noted. Because of the divergent response in cytokine expression in different cell types, more work needs to be done before a correlation between the cytokine gene expression and the pathogenesis of a disease can be made.

Animals↗
PubMed2004

Expression patterns of murine antichymotrypsin-like genes reflect evolutionary divergence at the Serpina3 locus.

Members of the serpin (serine protease inhibitor) superfamily of genes are well represented in both human and murine genomes. In many cases it is possible to identify a definite ortholog on the basis of sequence similarity and by examining the surrounding genes at syntenic loci. We have recently examined the murine serpin locus at 12F1 and observed that the single human alpha1-antichymotrypsin gene is represented by 14 paralogs. It is also known that the single human alpha1-antitrypsin gene has five paralogs in the mouse. The forces driving this gene multiplication are unknown and there are no data describing the function of the various serpin gene products at the alpha1-antichymotrypsin multigene locus. Examination of the predicted amino acid sequences shows that the serpins are likely to be functional protease inhibitors but with differing target protease specificities. In order to begin to address the question of the problem presented by the murine alpha1-antichymotrypsins, we have used RT-PCR to examine the expression pattern of these serpin genes. Our data show that the divergent reactive center loop sequence, and predictably variable target protease specificity, is reflected in tissue-specific expression for many of the family members. These observations add weight to the hypothesis that the antichymotrypsin-like serpins have an evolutionary importance which has led to their expansion and diversification in multiple species.

Animals↗
PubMed1992

The effect of thyroid hormone on fibronectin messenger ribonucleic acid levels in primary cultured rat hepatocytes.

Our previous in vivo studies demonstrated that thyroid hormone promotes the expression of the fibronectin (FN) gene in the rat liver, while it inhibits the synthesis in cultured human skin fibroblasts. These results can be interpreted as either different regulation of FN synthesis or gene expression among tissues, or divergent results of experiments performed in vivo or in vitro. Here we report on the action of thyroid hormone on FN gene expression in vitro using primary cultured hepatocytes compared to that in cultured skin fibroblasts. Hepatocytes were isolated from hypothyroid rats and were cultured in medium supplemented with thyroidectomized bovine serum (TxBS) or fetal bovine serum (FBS). T3 was added 2 or 24 h after plating, and cells were harvested after 2, 6, or 24 h. Total RNA was extracted, and mRNAs for rat FN and albumin were measured. The requirement of de novo protein synthesis for thyroid hormone-mediated induction of FN mRNA was examined by the addition of cycloheximide 15 min before T3 addition. The amount of FN mRNA significantly decreased in the hepatocytes cultured with TxBS compared with those cultured with FBS. The addition of T3 to TxBS resulted in the restoration of FN mRNA to the level in hepatocytes cultured in FBS. FN mRNA increased during the course of culture in the absence of T3; however, a further increase was observed 6 h after T3 addition. The abundance of albumin RNA decreased during the course of culture, but unlike FN mRNA, it was not changed by T3 addition. The increase in FN mRNA by T3 was not influenced by cycloheximide. These results indicate that thyroid hormone enhances FN gene expression in hepatocytes by its direct action without requiring de novo protein synthesis. In contrast, T3 decreased FN mRNA in cultured skin fibroblasts. Thus, the mode of thyroid hormone action on FN gene expression is different among tissues.

Animals↗
PubMed2001

HER2 protein expression and gene amplification in androgen-independent prostate cancer.

The role of the HER2 receptor remains uncertain in the pathogenesis and progression of human prostate cancer. Previous studies have reported widely divergent rates for HER2 expression in primary prostate tumors, probably owing to significant methodologic differences in the studies. Few data exist about the frequency of HER2 protein overexpression and gene amplification in androgen-independent prostate cancer (AIPC), although recent xenograft models suggest HER2 expression may be up-regulated in the transition from androgen-dependent to androgen-independent disease. We studied the role of HER2 protein in AIPC by immunohistochemical and fluorescence in situ hybridization (FISH) analyses on AIPC specimens using well-characterized and validated reagents. Fourteen (36%) of 39 specimens expressed HER2; however, only 2 (5%) had moderate (2+) expression, and 2 (5%) had high-level (3+) expression. Two (6%) of 36 specimens had gene amplification by FISH. These data suggest that HER2 protein overexpression and gene amplification are relatively uncommon in AIPC.

Adenoma↗
PubMed2005

Neurotrophic factor receptor expression and in vitro nerve growth of geniculate ganglion neurons that supply divergent nerves.

We investigated which neurotrophic factors may contribute to the divergence of two peripheral nerves emanating from the geniculate ganglion. We compared receptor mRNA profiles of the neurons that supply the nerves, and also the growth of their neurites in response to neurotrophic factors in culture. Three mRNAs, Gfra2, TrkA, and TrkC, were differentially expressed. Only one ligand, Neurturin, promoted substantially different nerve regrowth from the nerves, and therefore may contribute to nerve divergence. Three receptor mRNAs were expressed in 100% of the neurons: TrkB, TrkB.T2 (kinase-lacking isoform), and NCAM-140. Ligands for these Trks and FRalpha-1 promoted more outgrowth than ligands for the other receptors. NT-3 and BDNF synergistically promoted outgrowth. Finally, receptors are coexpressed at random rates, arguing against the existence of neuronal subtypes defined by a combinatorial code of these receptors.

Animals↗
PubMed1999

Novel characteristics and regulation of a divergent cinnamate 4-hydroxylase (CYP73A15) from French bean: engineering expression in yeast.

cDNAs showing high sequence similarity (>70%) over large stretches to plant CYP73A orthologues from other species were isolated from a cDNA library derived from mRNAs expressed in elicitor-treated suspension-cultured cells. These clones appear to code for a full-length 1554 bp open reading frame with a 78 bp 5'-untranslated region and a 140 bp 3'-untranslated region. The open reading frame, determined by sequence similarity, codes for a protein with a predicted Mr of 59229 and a pI of 8.8. It contains the conserved cysteine haem-binding site found in all cytochrome P450s. The protein encoded by this cDNA diverges however from other CYP73As in its N- and C-terminus and in four domains internally, so that overall sequence similarity is in the range 58-66%. Many clones contained an identical intron, which may be associated with a novel regulatory mechanism. Sequence similarity is sufficient for it to be classified as CYP73A15, although it is the least similar member of this family classified so far. The cDNA was expressed in yeast. Successful expression of cinnamate 4-hydroxylase activity required removal of the intron. High-level expression also required modification of the N-terminus to that of CYP73A1. Yeast did not process the intron at all and the leader sequence for A15 was not as compatible as that of A1. The mRNA for CYP73A15 was shown to be rapidly induced by elicitor treatment of suspension-cultured cells of French bean but induction was more transient than that of phenylalanine ammonia-lyase (PAL). In contrast, induction in cells undergoing xylogenesis was much more coordinate with PAL. The cloned cDNA may represent a cinnamate 4-hydroxylase isoform, whose expression is more related to differentiation than the responses to stress in which the majority of CYP73As cloned so far are involved.

Amino Acid Sequence↗
PubMed2004

Genetic analysis of the neuronal and ubiquitous AP-3 adaptor complexes reveals divergent functions in brain.

Neurons express adaptor (AP)-3 complexes assembled with either ubiquitous (beta3A) or neuronal-specific (beta3B) beta3 isoforms. However, it is unknown whether these complexes indeed perform distinct functions in neuronal tissue. Here, we explore this hypothesis by using genetically engineered mouse models lacking either beta3A- or beta3B-containing AP-3 complexes. Somatic and neurological phenotypes were specifically associated with the ubiquitous and neuronal adaptor deficiencies, respectively. At the cellular level, AP-3 isoforms were localized to distinct neuronal domains. beta3B-containing AP-3 complexes were preferentially targeted to neuronal processes. Consistently, beta3B deficiency compromised synaptic zinc stores assessed by Timm's staining and the synaptic vesicle targeting of membrane proteins involved in zinc uptake (ZnT3 and ClC-3). Surprisingly, despite the lack of neurological symptoms, beta3A-deficient mouse brain possessed significantly increased synaptic zinc stores and synaptic vesicle content of ZnT3 and ClC-3. These observations indicate that the functions of beta3A- and beta3B-containing complexes are distinct and divergent. Our results suggest that concerted nonredundant functions of neuronal and ubiquitous AP-3 provide a mechanism to control the levels of selected membrane proteins in synaptic vesicles.

Adaptor Protein Complex 3↗
PubMed2001

Gene expression and molecular evolution.

The combination of complete genome sequence information and estimates of mRNA abundances have begun to reveal causes of both silent and protein sequence evolution. Translational selection appears to explain patterns of synonymous codon usage in many prokaryotes as well as a number of eukaryotic model organisms (with the notable exception of vertebrates). Relationships between gene length and codon usage bias, however, remain unexplained. Intriguing correlations between expression patterns and protein divergence suggest some general mechanisms underlying protein evolution.

Animals↗
PubMed1996

Divergent effects of interleukin-1 beta on steroidogenesis and matrix metalloproteinase inhibitor expression and activity in cultured rat granulosa cells.

The periovulatory increase in ovarian matrix metalloproteinase inhibitor (MMPI) expression is regulated both in vitro and in vivo by LH, but the intermediary steps in this process are uncertain. The purpose of this experiment was to determine whether interleukin-1 beta (IL-1 beta), a known modulator of MMPI expression in other systems and one that is induced by LH in the ovary, is capable of regulating granulosa matrix metalloproteinase inhibitor expression and activity. Using an in vitro rat granulosa cell model, these parameters were assessed in response to IL-1 beta or LH administration alone or in combination. Granulosa cells were obtained from 24-day-old immature female rats primed with 20 IU PMSG at 22 days of age. Cells were cultured under serum-free conditions for 24 h at 37 C in the presence of medium (control), LH (100 ng/ml), IL-1 beta (10 ng/ml), or LH plus IL-1 beta. MMPI activity in the conditioned medium was assessed using a colorimetric assay (n = 6), whereas progesterone and estrogen concentrations in the conditioned medium were determined by RIA (n = 6). RNA was isolated from the granulosa cells and assessed for Northern analysis of tissue inhibitor of metalloproteinase-1 (TIMP-1; n = 4), TIMP-2 (n = 3), and TIMP-3 (n = 3) expression. When added to granulosa cells, IL-1 beta and LH each significantly (P < 0.05) increased MMPI activity in granulosa cell-conditioned medium above control values (40.9 +/- 3.0% inhibition for IL-1 beta and 67.1 +/- 5.6% inhibition for LH vs. 31.4 +/- 2.4% inhibition for controls). When added in combination, IL-1 beta had no effect on LH-stimulated inhibitor activity (67.1 +/- 5.6% inhibition vs. 69.9 +/- 5.1% inhibition for LH and LH plus IL-1 beta, respectively). Methylamine hydrochloride treatment revealed that the majority of inhibitor activity in all treatment groups was derived from TIMPs. The patterns of TIMP-1, TIMP-2, and TIMP-3 messenger RNA expression among the treatment groups paralleled the TIMP-derived inhibitor activity, in that both IL-1 beta and LH alone stimulated transcript expression of all three TIMPs. In addition, an increase in progesterone production was associated with IL-1 beta-stimulated (1.22-fold over control values; P = 0.0006) and LH-stimulated (9.6-fold over control values; P = 0.007) MMPI expression and activity. Lastly, IL-1 beta and LH significantly (P < 0.05) decreased estrogen production by approximately 33% compared to that in cultures with LH only. It is concluded from the current study that IL-1 beta is a mediator of MMPI expression as well as granulosa cell steroidogenesis, and that this cytokine has divergent actions in the presence and absence of LH.

Animals↗
PubMed1994

Neural selective activation and temporal regulation of a mammalian GAP-43 promoter in zebrafish.

Neurons throughout the vertebrate nervous system selectively activate the gene for a growth cone component, GAP-43, during embryonic development, and then decrease its expression abruptly as they form synapses. Distal interruption of mature axons in the central nervous system (CNS) of fish and amphibians, but not in the mammalian CNS reverses the developmental down-regulation of GAP-43 expression. To explore functional conservation and divergence of cis-acting elements that regulate expression of the GAP-43 gene, we studied activation, in transgenic zebrafish embryos, of mammalian GAP-43 genomic sequences fused to a marker gene. The DNA fragments containing the GAP-43 promoter, including a short fragment of 386 base pairs, were preferentially activated in the embryonic fish nervous system at times when extensive neuronal differentiation and neurite outgrowth take place. After 2 days of development, expression of the mammalian transgenes was specifically downregulated in the fish spinal cord but increased in more rostral regions of the CNS. This expression pattern was well correlated with the regulation of the endogenous fish GAP-43 gene revealed by in situ hybridization. Elements of the mammalian gene located a substantial distance upstream of the minimal promoter directed additional expression of the marker gene in a specific set of non-neural cells in zebrafish embryos. Our results indicate that cis-acting elements of the GAP-43 gene, and signaling pathways controlling these elements during embryonic development, have been functionally conserved in vertebrate evolution.

Animals↗
PubMed1992

Comparisons of the effects of TCDD and hydrocortisone on growth factor expression provide insight into their interaction in the embryonic mouse palate.

Cleft palate (CP) can be induced in embryonic mice by a wide range of compounds, including glucocorticoids and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Hydrocortisone (HC), a glucocorticoid, retards embryonic growth producing small palatal shelves, while TCDD exposure blocks the fusion of normally sized shelves. TCDD induction of CP involves altered differentiation of the medial epithelial cells. Recent studies indicate that growth factors such as EGF, TGF-alpha, TGF-beta 1, and TGF-beta 2 are involved in palatogenesis, regulating proliferation, differentiation, and extracellular matrix production. A synergism has been observed between HC and TCDD in which doses too low to induce CP alone are able to produce greater than 90% incidence when coadministered. In the present study a standard teratology protocol was performed in C57BL/6N mice to examine the synergism at doses lower than those previously published. Data from this study indicate synergistic interactions at doses as low as 3 micrograms TCDD/kg + 1 mg HC/kg. This extreme sensitivity suggests the involvement of a receptor-mediated mechanism possibly resulting in altered regulation of gene expression. Mechanisms of interaction were further studied by comparing growth of the shelves, fate of the medial epithelium, and expression of growth factor mRNAs and peptides. Pregnant mice were dosed on GDs 10-13 with HC (100 mg/kg sc) or with HC (25 mg/kg sc) + TCDD (3 micrograms/kg orally), doses producing 30% and 99% CP, respectively. The interaction between HC and TCDD results in a small HC-like palate, rather than the morphology typical of TCDD-induced clefting. Both compounds inhibited programmed cell death of the medial epithelium, which instead differentiated into an oral-like epithelium. The alterations in growth factor expression after HC or HC + TCDD were similar. Expression of EGF, TGF-beta 1, TGF-beta 2, and EGF receptor increased in specific palatal regions. Increased levels of mRNA were observed only for TGF-beta 1. The effect of TCDD alone on growth factor expression differ from those seen with HC or HC + TCDD. These divergent effects on growth factor expression may contribute to the differences in shelf size and thus to the different mechanisms of HC and TCDD clefting. Thus the synergism between HC and TCDD may involve similar and potentially additive effects on regulators of proliferation and differentiation in the palate, but additional contributing factors cannot be excluded.

Animals↗
PubMed2026

Identification and differential regulation of proteasome &#x3b2; family genes by viral infection and cytokines in grass carp (Ctenopharyngodon idella).

Proteasome &#x3b2; (PSMB) subunits are essential components of the proteasome complex and play important roles in antigen processing and immune regulation. In this study, we identified 14 Psmb genes in grass carp (Ctenopharyngodon idella), including seven constitutive Psmbs (Psmb1-7), three immunoproteasome genes (Psmb8-10), two thymoproteasome-related paralogs (Psmb11a and Psmb11b), and two telelost-specific members (Psmb12 and Psmb13). Comparative genomic analyses showed that grass carp Psmb genes are highly conserved in genomic organization, gene synteny, and predicted &#x3b2;-subunit-like protein structures, supporting the evolutionary conservation of the proteasome &#x3b2;-subunit family in fish. Phylogenetic and syntenic analyses further revealed lineage-specific expansion of immunoproteasome-related Psmb genes in teleost fish, with Psmb12 and Psmb13 likely derived from duplications of Psmb9 and Psmb10, respectively. Tissue expression analysis suggested functional divergence among duplicated Psmb members, as constitutive Psmbs were relatively enriched in the brain, whereas immunoproteasome-related and teleost-specific Psmbs were highly expressed in immune- and mucosa-associated tissues. Moreover, GCRV-I infection rapidly induced Psmb8-10 and Psmb11b expression in CIK cells. IFN-&#x3b3; induced a broader set of Psmb genes than IFNa, whereas IL-10 selectively suppressed several Psmbs. Together, these findings highlight the evolutionary conservation, expansion, and immune-related diversification of the Psmb family in teleost fish.

Animals↗
PubMed1996

Characterization of a novel member of the macrophage mannose receptor type C lectin family.

The recognition of a diversity of carbohydrates by the various calcium dependent (type C) lectin family members has been shown to be critical for a variety of processes ranging from cell adhesion to antigen presentation. Examination of the expressed sequence tag (EST) data base for novel type C lectins using E-selectin as a probe resulted in the identification of a distantly related short polypeptide sequence containing many of the conserved residues found in these carbohydrate-binding proteins. Cloning of the full-length murine cDNA containing this region revealed that this protein is a novel member of the family that includes the macrophage mannose, the phospholipase A2, and the DEC 205 receptors, with a cysteine-rich domain, a fibronectin type 2 domain, eight type C lectin domains, a transmembrane domain, and a short cytoplasmic carboxyl terminus. Genomic Southern analysis suggests that this is a conserved protein, and examination of a human homologue revealed a high degree of sequence homology with the murine form. Northern blot analysis revealed expression of a large transcript in a number of different human and murine tissues and tumor cells and an alternatively spliced smaller transcript with a divergent 5' sequence was expressed specifically in the human fetal liver. Analysis of the genomic structure revealed that the gene encoding this lectin was interrupted by a large number of introns, and the intron structure was similar to the macrophage mannose receptor gene. Finally, in situ hybridization analysis demonstrated that the transcript encoding this lectin was found in a number of highly endothelialized sites as well as in chondrocytes in cartilaginous regions of the embryo.

Amino Acid Sequence↗
PubMed1996

Conservation of function and expression of unc-119 from two Caenorhabditis species despite divergence of non-coding DNA.

The Caenorhabditis briggsae homologue of the Caenorhabditis elegans neuronal gene unc-119 has been cloned by low-stringency hybridization. Genomic clones containing the C. briggsae gene are able to completely rescue the unc-119 phenotype in transgenic C. elegans mutants. The open reading frame (ORF) of the predicted C. briggsae cDNA is 90% identical to that of C. elegans. Although the splice donor and acceptor sites are conserved, the untranslated regions, and the introns, differ greatly. For this gene, the average intron size in C. elegans is over 600 base pairs (bp); in C. briggsae it is only 113 bp. Their upstream control regions share limited sequence similarities; however, reporter gene fusions of the two species show strongly similar expression in C. elegans. These results are consistent with the maintenance not only of the function of the unc-119 gene but also the transcriptional control of the gene through tens of millions of years of evolution.

Amino Acid Sequence↗
PubMedDate not supplied

Progesterone receptor repression by estrogens in rat uterine epithelial cells.

Measurements performed using cell lines or animal tissues have shown that the progesterone receptor (PR) can be induced by estrogens. By use of immunohistochemistry we studied the effects of estrogens on the PR levels in the individual cell types of the target organs uterus and breast. In the uteri of rats, ovariectomy induced a decrease in PR immunoreactivity within the myometrium and outer stromal cell layers. In contrast, in the uterine luminal and glandular epithelium and surrounding stromal cell layers the PR immunoreactivity was significantly enhanced. The same picture emerged when intact rats were treated with the pure estrogen receptor antagonist, ZM 182780 (10 mg/kg/d). Treatment of ovariectomized rats with estradiol resulted in high PR levels in the myometrium and stroma cells but low PR immunoreactivity in the epithelial cells. The ER-mediated repression of the PR immunoreactivity was evidently restricted to the uterine epithelium, as we found that in the epithelial cells of the mammary gland and in cells of N-nitrosomethylurea-induced mammary carcinomas the PR expression was induced by estrogens and was blocked by the pure antiestrogen ZM 182780. These results clearly show that in the rat the activated ER induces diverging effects on PR expression in different cell types even within the same organ.

Animals↗
PubMed1994

Activity-dependent regulation of N-methyl-D-aspartate receptor subunit expression in rat cerebellar granule cells.

The glutamate receptor channels of the N-methyl-D-aspartate (NMDA) subtype are composed of different subunits named NR1 and NR2A-D. These subunits can combine in different oligomers with diverging properties and their expression is developmentally regulated. We have used rat cerebellar slice cultures to test the involvement of bioelectrical activity and synaptic transmission in the changes in NR2A-C expression observed in developing granule cells. A correlation between the functional properties of the NMDA receptors and expression of the NR2A-C mRNAs was obtained in single granule cells by coupling patch-clamp recording and reverse transcription followed by polymerase chain reaction. Granule cells grown under standard culture conditions expressed mainly NR2A mRNA when examined after 15-40 days in vitro. Consistent with this observation, their responses to NMDA were only weakly reduced by 3 microM ifenprodil, a non-competitive antagonist which discriminates between NR2A and NR2B subunits in expression systems. In cerebellar cultures chronically exposed to tetrodotoxin to eliminate spontaneous electrical activity, granule cells maintained a predominant expression of NR2B subunits and their responses to NMDA were largely inhibited by 3 microM ifenprodil. These results provide evidence that the expression of the NR2A and B subunits is regulated through an activity-dependent mechanism leading to the formation of NMDA receptors with different pharmacological properties. Finally, the NR2C subunit, abundantly expressed in vivo by adult granule cells, was only rarely detected in slice cultures, even when excitatory synapses were formed between granule cells and fibres originating from co-cultured brainstem explants. These data suggest that the induction of NR2C expression observed in vivo requires an additional factor(s) that remains to be identified.

Animals↗