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PubMed1989

IL-4 induces LFA-1 and LFA-3 expression on Burkitt's lymphoma cell lines. Requirement of additional activation by phorbol myristate acetate for induction of homotypic cell adhesions.

LFA-1 and LFA-3 expression is absent or low on Burkitt's lymphoma cell lines and low on the EBV-transformed B cell line UD61. Incubation of cells of BL2 and of UD61 with various concentrations of IL-4 resulted in induction of LFA-1 and LFA-3 expression in a dose dependent fashion. This effect was already observed after 16 h of incubation whereas maximal expression was obtained after 72 h. Induction of LFA-1 and LFA-3 expression seemed to be specific for IL-4, because IL-1, IL-2, IL-3, IFN-alpha, IFN-gamma and a low m.w. B cell growth factor were ineffective. LFA-1 and LFA-3 induction by IL-4 was blocked specifically by an anti-IL-4 antiserum. Induction of LFA-1 expression by IL-4 was furthermore confirmed at the specific LFA-1 beta-chain mRNA level. IL-4 was unable to induce LFA-1 expression on EBV-transformed lymphoblastoid cell lines of two LFA-1-deficient patients. BL2 grows as single cells, but induction of LFA-1 and LFA-3 expression by IL-4 was insufficient to induce homotypic cell adhesions and required PMA as a second signal. PMA alone did not induce LFA-1 antigen expression and was unable to induce adhesions between BL2 cells in the absence of IL-4 in 22 h assays. Addition of PMA to BL2 cells that expressed LFA-1 Ag upon incubation with IL-4 resulted in aggregate formation within 30 min. Adhesions between BL2 cells induced by IL-4 in combination with PMA were blocked by anti-LFA-1 beta or anti-LFA-1 alpha-chains mAb. In addition, these mAbs dispersed preformed aggregates of BL2 cells. Our results indicate that IL-4 can induce the adhesion molecules LFA-1 and LFA-3 on B cell lines, but that an additional activation signal provided by PMA was required for the induction of homotypic cell adhesions.

Antibodies, Monoclonal↗
PubMed1986

The repetitive structure of the profilaggrin gene as demonstrated using epidermal profilaggrin cDNA.

Filaggrin is the histidine-rich basic protein that aggregates keratin filaments in fully differentiated cells of the epidermis. Filaggrin is synthesized in the granular cell layer as a high molecular weight precursor protein (profilaggrin) that consists of multiple repeated copies of filaggrin. cDNA clones for rat and mouse epidermal profilaggrin have been constructed from sucrose gradient-enriched RNA in order to study the repetitive structure of profilaggrin. These clones hybridize to high molecular weight epidermal mRNA (23 kilobase pairs, rat and 19 kilobase pairs, mouse) and exhibit limited cross-hybridization between species. Several rat clones direct the synthesis of a portion of rat profilaggrin in bacteria. One of these, rat profilaggrin cDNA clone R4D6, is 2400 base pairs in length. The R4D6 cDNA is shown to contain repetitive sequence by restriction mapping and southern hybridization analysis of restriction digests of this plasmid, using subfragments of the plasmid as hybridization probes. Southern hybridization analysis of rat genomic DNA, digested to completion with several restriction enzymes, reveals a simple hybridization pattern of fragments equal in size to those of the cDNA. Partial digestion of rat genomic DNA results in a ladder of bands based on a 1200-base pair repeat, equal to the size of the repeating unit of the cDNA clone, and consistent with the expected repeating size of profilaggrin. Together, these results show that the profilaggrin mRNA and gene have repetitive structure and that the gene apparently lacks introns in the coding region.

Amino Acid Sequence↗
PubMed1994

Modulation of Fc receptors for IgG on bovine polymorphonuclear neutrophils by interferon-gamma through de novo RNA transcription and protein synthesis.

Polymorphonuclear neutrophils (PMN) from 4 cows were preincubated (30 minutes, 37 C) in either actinomycin D (100 micrograms/ml) or puromycin (10 micrograms/ml), inhibitors of mRNA transcription and protein translation, or in medium 199. The PMN were incubated for a further 4.5 hours in medium containing 100 U of recombinant bovine interferon-gamma (rboIfn-gamma). The PMN were then incubated with bovine IgG1, IgG2, IgM, or aggregated IgG (aIgG; 4 C, 12 hours) for flow cytometric analysis, using fluoresceinated isotype-specific antibody. The percentage of PMN binding the ligand and the logarithmic mean fluorescent channel (LMFC), an indicator of the amount of receptor (R) expression, were recorded. Competitive inhibition of ligand binding was measured by incubating PMN with fluoresceinated IgG2 in the presence or absence of 100-fold excess of IgG1, IgG2, and aIgG. Activation with rboIfn-gamma induced a 4.5-fold increase in binding of IgG1 and a fivefold increase in LMFC for IgG2. These increases were inhibited by actinomycin D and puromycin. Percentage of PMN binding aIgG decreased after activation by rboIfn-gamma. Interferon-gamma treatment did not affect binding or LMFC of IgM. However, binding of IgM was reduced by treatment with actinomycin D. Binding of fluoresceinated IgG2 was inhibited by unlabeled IgG1, IgG2, and aIgG. Results indicate that bovine PMN Fc receptors (FcR) for IgG1 and IgG2 were rboIfn-gamma inducible, that induction required de novo transcription and translation, that a heterogeneous population of FcR exist on bovine PMN, and that IgG1 and IgG2 share a common FcR. Further, bovine PMN are capable of gene activation and are responsive to changes in their environment, thus being amenable to modulation for effective pathogen destruction.

Animals↗
PubMed1988

Deactivation of gene expression upon the onset of development in dictyostelium discoideum.

Several genes that are deactivated upon the initiation of development of Dictyostelium discoideum have been identified by differential screening of various cDNA libraries. These genes have in common a decrease in the steady-state levels of their corresponding mRNAs as development proceeds. When development was carried out in the absence of protein synthesis by inhibition with cycloheximide, the decrease in mRNA levels for most genes (V genes) was normal or slightly accelerated. However, for about 5% of the genes (H genes), cycloheximide caused an apparent induction of expression, as revealed by a slight or dramatic increase in mRNA levels instead of the normal decrease. This effect was due to inhibition of protein synthesis and not to cycloheximide per se. The induction was found to be due to an enhancement of the transcription rate; normal rates of transcription for the H genes were dependent upon continued protein synthesis during vegetative growth and during development. Thus, two general regulatory classes exist for deactivation of gene expression upon initiation of development, one dependent and one independent of protein synthesis. Models concerning the control of expression of these two classes of genes are discussed here. Analysis of expression of these genes in mutant strains that are aggregation-deficient has also been performed, and the results lead to subdivisions of the classes.

Cycloheximide↗
PubMed1983

DNA-binding properties of the Erf protein of bacteriophage P22.

The phage P22 erf (essential recombination function) gene was placed in a small plasmid under the control of a strong, inducible promoter by manipulations in vitro. Erf protein was purified from induced cells, and characterized. Erf protein (monomer molecular weight 23,000) forms oligomers in solution. The carboxyl terminus is protease-sensitive: its removal generates a discrete amino-terminal fragment (molecular weight approximately 18,000) that also oligomerizes. At temperatures below 45 degrees C, Erf forms stable, discrete complexes with single-stranded DNA and supercoiled DNA, but not with relaxed double-stranded DNA. Binding to single-stranded DNA is stoichiometric; one Erf monomer binds approximately 15 bases of DNA, over the range of protein concentrations tested (2 to 100 micrograms/ml). At high temperatures (50 to 60 degrees C). Erf binds single- and double-stranded DNA, forming aggregates instead of discrete complexes. Heating and cooling in the absence of DNA produces a form of Erf that has single-stranded binding specificity, but forms aggregates on binding.

DNA Helicases↗
PubMed1994

Response of striatal astrocytes to neuronal deafferentation: an immunocytochemical and ultrastructural study.

This ultrastructural and light microscopic immunocytochemical study describes the time course of anatomical changes that occur in striatal astrocytes in response to neuronal deafferentation in young adult rats and the coordinate distribution of two astrocytic proteins involved in reactive synaptogenesis, glial fibrillary acidic protein and clusterin. We found that following a unilateral lesion of the cerebral cortex, striatal astrocytes undergo a rapid ultrastructural transformation from a protoplasmic to a reactive type of astroglia and are the primary cells involved in the removal of degenerating axon terminals, but not axons of passage, from the neuropil. In addition, at 10 and 27 days postlesion, processes of reactive astrocytes are also seen to occupy vacant postsynaptic spines after degenerating presynaptic terminals are removed, suggesting that they may also participate in the reinnervation of the deafferented neurons. By immunocytochemistry, reactive astrocytes were characterized by a significant increase in the intensity of glial fibrillary acidic protein staining beginning at three days postlesion and lasting for at least 27 days postlesion. Reactive astrocytes were characterized by cellular hypertrophy and an increase in the density of immunoreactive processes distributed throughout the deafferented striatum. However, our analysis of astrocyte cell number found no evidence of astrocyte proliferation in response to the deafferentation lesion. Although previous in situ hybridization studies have reported elevated clusterin messenger RNA in reactive astrocytes after decortication, clusterin immunoreactivity was not seen in the cell soma of reactive astrocytes but was distributed as punctate deposits, ranging from 1 to 2 microns in diameter, within the neuropil of the deafferented striatum. At 10 days postlesion, the distribution of clusterin staining appeared as large aggregates of immunoreactive deposits adjacent to neurons. However, by 27 days postlesion, the aggregates of clusterin reaction product were replaced by a fine scattering of individual punctate deposits distributed evenly over the dorsal part of the deafferented striatum. These data support the notion that reactive astrocytes serve multiple, time-dependent roles in response to brain injury and are involved in both the removal of degenerative debris from the lesion site as well as in reforming the synaptic circuitry of the damaged brain. Our data suggest that, in response to decortication, reactive astrocytes are the primary cells responsible for removing degenerating axon terminals, but not axons of passage, from the deafferented striatum and that the coordinate increase in glial fibrillary acidic protein may serve to stabilize the extension of reactive astrocytic processes during phagocytosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1995

Persistent activation of min K channels by chemical cross-linking.

Expression of the structurally and functionally distinct min K channel in Xenopus oocytes results in voltage-dependent potassium currents that activate with a characteristic slow time course. Application of a membrane-impermeable chemical cross-linking agent to oocytes expressing min K decreased the time-dependent current, increased its rate of activation, and induced persistently activated inward and outward potassium currents. These effects required membrane depolarization, demonstrating use dependence. Persistently activated channels retained potassium selectivity and sensitivity to block by clofilium and barium. These results suggest that a major conformational change occurs during min K channel gating, which can be stabilized by chemical cross-linking, and are consistent with a model in which min K channels activate by voltage-dependent subunit aggregation.

Animals↗
PubMed2005

Leptin potentiates ADP-induced [Ca(2+)](i) increase via JAK2 and tyrosine kinases in a megakaryoblast cell line.

Plasma leptin levels are elevated in most of obese individuals, and obesity is associated with high incidence of cardiovascular diseases. It has been reported that leptin is an independent risk factor for the coronary artery disease in obese patients and that leptin is involved in the pathogenesis of cardiovascular diseases. We previously reported that leptin promotes platelet aggregation. The present study aimed to elucidate the mechanisms underlying this effect of leptin using a megakaryoblast cell line, MEG-01 cells. Leptin receptors mRNAs expression in MEG-01 cells were analyzed by RT-PCR. Leptin-induced tyrosine-phosphorylation of proteins was analyzed by immunoblotting with an anti-phosphotyrosine antibody. ADP-induced increases in cytosolic Ca(2+) concentration ([Ca(2+)](i)) in the presence and absence of leptin were measured by dual-wavelength fura-2 microfluorometry. Both Ob-Ra and Ob-Rb, were expressed and leptin-induced tyrosine-phosphorylation of several proteins in MEG-01 cells. Leptin-potentiated increases in [Ca(2+)](i) induced by ADP. ADP at a subthreshold concentration and leptin acted synergistically in producing [Ca(2+)](i) increases. These effects of leptin on [Ca(2+)](i) were inhibited by blockers of JAK2 and tyrosine kinases. Furthermore, leptin increased the tyrosine-phosphorylation of Gq alpha-subunits. The results indicate that leptin enhances ADP-induced [Ca(2+)](i) increases via JAK2 and tyrosine kinases in a megakaryoblast cell line. This mechanism may underlie the potentiation of platelet aggregation by leptin.

Adenosine Diphosphate↗
PubMed2006

Identification of calreticulin as a marker for phagocytosis of apoptotic cells in Drosophila.

Apoptotic cell phagocytosis is initiated through the specific interaction between markers for phagocytosis present at the surface of targets and their receptors of phagocytes. Although many molecules have been proposed to be phagocytosis markers and receptors in mammals, information as to the identity of those molecules is limited for invertebrate animals. Calreticulin, a molecular chaperone that functions in the lumen of the endoplasmic reticulum, was recently reported to be the second general marker, the membrane phospholipid phosphatidylserine being the first, for mammalian apoptotic cells to be recognized by phagocytes. We here asked whether or not calreticulin serves as a marker for phagocytosis in Drosophila. Phagocytosis of apoptotic S2 cells by Drosophila hemocyte-derived l(2)mbn cells, which we previously showed to occur independent of phosphatidylserine, was inhibited by the addition of anti-calreticulin antibody. This inhibition was observed when the target cells, but not phagocytes, were pre-incubated with the antibody. In addition, RNA interference-mediated reduction of calreticulin expression in apoptotic S2 cells, but not in l(2)mbn cells, reduced the level of phagocytosis. An immunocytochemical analysis revealed that calreticulin is widely distributed at the surface of viable S2 cells. After the induction of apoptosis, cell surface calreticulin seemed to form aggregates, with no change in its amount. Furthermore, in embryos of a mutant Drosophila strain that expresses calreticulin at a reduced level, the level of phagocytosis of apoptotic cells was about a half of that observed in embryos of a wild-type strain. These results collectively indicate that calreticulin is the first molecule to be identified as a marker for phagocytosis of apoptotic cells by Drosophila phagocytes.

Animals↗
PubMed1987

Effect of oxygen on levels of mRNA coding for reaction-centre and light-harvesting polypeptides of Rhodobacter sphaeroides.

The relative levels of mRNA for the reaction-centre L and M subunits, B875 (LH1) alpha and beta polypeptides and B800-850 (LH2) alpha and beta polypeptides, have been measured during pigment induction of Rhodobacter sphaeroides. Over the 6 h of the experiment, bacteriochlorophyll levels increased by at least 100-fold. No transcripts for photosynthetic components were detectable at the start of induction; after 2 h the levels of transcripts from the puf operon (encoding reaction-centre and B875 subunits) had reached the maximum; these transcripts were 2.7 and 0.5 kb respectively. The transcript for the puc operon (B800-850 complex) was estimated to be 0.55 kb and reached a maximum level after 6 h. These results are consistent with the proposal that, during the assembly of the photosynthetic apparatus, the synthesis of B875 reaction-centre aggregates precedes that of the major antenna, B800-850.

Bacterial Proteins↗
PubMed2006

Cdk5 regulates STAT3 activation and cell proliferation in medullary thyroid carcinoma cells.

The biological behaviors of thyroid cancer are varied, and the pathological mechanisms remain unclear. Some reports indicated an apparent aggregation of amyloid accompanying medullary thyroid carcinoma (MTC). Amyloid aggregation in neurodegeneration leads to hyperactivation of Cdk5 and subsequent neuronal death. Based on the connection with amyloid, the role of Cdk5 in MTC is worthy of investigation. Initially, the expression of Cdk5 and its activator, p35, in MTC cell lines was identified. Cdk5 inhibition by specific inhibitors or short interfering RNA decreased the proliferation of MTC cell lines, which reveals the importance of Cdk5 in MTC cell growth. Although p35 cleavage has been considered as an important element in neurodegeneration, it seems that p35 cleavage was not a major cause in Cdk5 activity-dependent MTC cell proliferation because neither Cdk5 activity nor cell growth was affected by the inhibition of p35 cleavage. Clearance of amyloid by antibody neutralization indicated that MTC cell proliferation was supported by calcitonin-derived extracellular amyloid and subsequent Her2 and Cdk5 activation. Significantly, the STAT3 pathway was involved in Cdk5-dependent proliferation of MTC cells through Ser-727 phosphorylation. In addition, Cdk5 inhibition reduced nuclear distributions of both the Cdk5-p35 complex and phospho-STAT3 in MTC cells. Finally, Cdk5 inhibition retarded tumor formation in vivo accompanying the reduction of phospho-STAT3. Our findings suggest the first demonstration of a novel and specific role for Cdk5 kinase in supporting the proliferation of the medullary thyroid carcinoma cells and could shed light on a new field for diagnosis and therapy of thyroid cancer.

Animals↗
PubMed2004

Purification, gene cloning and expression of an acidic phospholipase A2 from Agkistrodon shedaoensis Zhao.

A protein with the activity of phospholipase A(2) named asAPLA(2) was purified to homogeneity from the venom of Agkistrodon shedaoensis Zhao through DEAE-Sepharose CL-6B anion exchange column, Source S, and Mono Q FPLC. Its molecular weight was estimated to be 19 kD by SDS-PAGE, and its pI was about 3.5 by IEF analysis. It inhibited the platelet aggregation that was induced by 1 micromol/ L ADP, and the IC(50) was determined to be 6 micromol/L. Degenerating primer was designed and synthesized according to the N-terminal amino acid sequence of asAPLA(2). Its full-length cDNA was cloned by RT-PCR from the total RNA extracted from the snake venom gland. Its molecular weight and the pI are determined to be 13,649 and 4.39 respectively as calculated by DNAclub and DNAstar software according to the deduced amino acid sequence. Then the gene was cloned into the expression plasmid pET-40b(+) and expressed in E. coli BL21(DE3). Western blot analysis indicated that the expressed protein cross-reacted with the antibody against the native enzyme.

Agkistrodon↗
PubMed2004

Complete sequence of a picorna-like virus of the genus Iflavirus replicating in the mite Varroa destructor.

Aggregations of 27 nm virus-like particles were observed in electron microscopy images of sectioned Varroa destructor mite tissue. The scattered occurrence of individual particles and accumulation of the virions in lattices in the cytoplasm gave an apparent indication that the virus replicates in the mite. Sequence analysis of the RNA of the purified virus revealed a genome organization with high similarity to that of members of the genus Iflavirus. Phylogenetic analysis of the polymerase showed that the virus was related most closely to Deformed wing virus (DWV) and Kakugo virus (KV) of bees. The virus has a genome of 10 112 nt without the poly(A) tail, with an overall RNA genome identity of 84 % to those of DWV and KV and has one large ORF, translated into a 2893 aa polyprotein with an amino acid identity of 95 % to those of DWV and KV. The first 1455 nt of the ORF encoding the lower molecular mass structural proteins shows the greatest diversion from those of DWV and KV, with an RNA identity of 79 %, and translates to a polypeptide of 485 aa with an identity of 90 %. The name proposed for this virus is Varroa destructor virus 1 (VDV-1). To determine whether VDV-1 replicates in mites, a selective RT-PCR was done to detect the presence of the negative-sense RNA strand. The virus isolate and the closely related DWV could be discriminated by two primer sets, each specific to one virus. Both viruses replicated in the population of the mite species studied.

Amino Acid Sequence↗
PubMed1989

Effect of divalent cations on structure-function relationships of the antitumor protein alpha-sarcin.

alpha-Sarcin binds one Zn(II) cation per protein molecule, with a Kd value of 0.9 mM, determined by equilibrium dialysis experiments. Ca(II), Mg(II), and Mn(II) do not bind to alpha-sarcin. Cd(II) and Co(II) also behave as Zn(II). The binding produces local modifications on the protein conformation affecting the microenvironment of tryptophan residues. The three cations modify the fluorescence emission of the protein. The near-u.v. circular dichroism spectrum of the protein is also altered. The binding of Zn(II) and related cations does not modify the secondary structure of the protein. The ribonucleolytic activity of alpha-sarcin is inhibited upon Zn(II) binding, but no alteration of the ability of the protein to aggregate phospholipid vesicles has been observed.

Antineoplastic Agents↗
PubMed1974

Intracellular virus-specific structures and RNAs in oncornavirus-producing human cells.

Two kinds of virus-specific structures were isolated from the cytoplasm of Detroit-6 and human amnion cells producing oncornavirus-like particles. These structures represented A particles with the diameter of 70 to 80 nm and aggregated strands of nucleocapsids with the diameter of 3 and 6 nm. The structures were separated from cellular contaminants by isopycnic banding in linear sucrose gradients and subsequently further purified by sedimentation in velocity sucrose gradients. Their sedimentation coefficient was 250 and 150S, respectively. Both structures contain 60, 45, and 35S RNA species, and 150S structures also contained 20S RNA. The 35 and 20S RNA from the 150S structure formed hybrids with DNA enzymatically synthesized on extracellular virions. The structures displayed endogeneous polymerase activity, DNA product of the reaction being predominantly associated with 60S RNA. No 70S RNA was found in the cell structures of various densities. Also, the virions purified from tissue culture fluid contained 70S RNA. These findings are consistent with those on extracellular maturation of oncornavirus RNA.

Amnion↗
PubMed2003

Monitoring of microbial diversity by fluorescence in situ hybridization and fluorescence spectrometry.

The goal of the research was the development of a simple method to quantify microbial groups in environmental samples. Fluorescence intensity was measured in the sample before and after whole cell fluorescence in situ hybridization with rRNA-targeted, fluorochrome-labeled oligonucleotide probes. To determine specific and non-specific binding of different oligonucleotide probes the following approaches have been used: (1) incubation of the sample with probes at two different temperatures; (2) hybridization of labeled probe in the presence of unlabeled probe; (3) incubation of the sample with labeled specific probe or labeled nonsense probe. Specific binding (hybridization) of the probe was calculated as the difference between total binding and non-specific binding of the probe. Specific binding was 40-50% of total binding in the environmental samples tested. The ratio of the specific binding of different probes may be used to quantify the ratio of different microbial groups in the environmental samples. This quantification is suitable for the microbiological monitoring of microbial aggregates because it is a simple technique and the results can be measured by a portable fluorometer.

Bacteria↗
PubMed2004

[Interface domain of hepatitis E virus capsid protein homodimer].

Hepatitis E is a main cause of acute viral hepatitis in developing countries where it occurs as sporadic cases and in epidemics form. The causative agent, hepatitis E virus, is transmitted primarily by the fecal-oral route. The approximately 7.5 kb positive-sense single-strand RNA genome includes three open reading frames (ORFs), one of which (ORF2) is postulated to encode the major viral capsid protein (pORF2) of 660 amino acid residues. We earlier showed that a bacterially expressed peptide, designated as NE2, located from amino acid residues 394 to 606 of ORF2, was found to aggregate into homodimer to at least hexamer. To understand the interface domains within this peptide vital for dimerization and formation of major neutralizing epitopes, NE2 protein underwent terminal-truncated and site-directed mutation. The hydrophobic region, ORF2 aa597-aa602 (AVAVLA), played a key role in oligomerization. Any amino acid residue of this region replaced with glutamic acid residue, the peptide can not refold as homodimer and/or oligomer. The immunoreactivities of these mutant peptides, blotted with anti-HEV neutralizing monoclonal antibody (8C11) and convalescent human sera, show associated to the formation of homodimer. The intermolecular contact region on homodimer was investigated by chemical cross-linking of two site-directed cysteines. When the alanine on aa597 site mutated with cysteine, two different homodimers were found in SDS-PAGE analysis. One (42kD) can be disassociated with 8mol/L urea, which is postulated to form by virtue of hydrophobic interaction, and the other (60kD) falls apart with the reductant DTT present. The exact conformation, generating the cross-linking reaction of cysteines, was further investigated by induced-oxidation on monomer and hydrophobic homodimer of A597C protein with GSH/GSSG. And the results revealed, it is the conformation of hydrophobic homodimer that induces the disulfide bond come into being, instead of the one of monomer. So the aa597 site was verified to be located on interface domain of hydrophobically interacting homodimeric complex. To evaluate the biological significance of hydrophobicity of interface domain, we searched natural variations as to the region on all available databases with NCBI blast program. All variations on these amino acid residues kept higher hydrophobicity, which suggests that the hydrophobic domain is critical for the assemblage and propagation of HEV. NE2 N-terminal deletions up to aa458 had no effect on dimerization and took no exact part in formation of major neutralizing epitopes, but the fragment may act as helper for the formation of major neutralizing epitopes on NE2. Interestingly, the C-terminus aa605-aa660 of ORF2 can also act as helper instead of the N-terminus of NE2. This study suggests an interface domain of NE2 might be vital for HEV capsomer assembly and formation of major neutralizing epitopes. These results may offer clues to the rational design of recombinant anti-HEV vaccine.

Capsid Proteins↗
PubMed1991

The expression of IGF-II in the early post-implantation rat conceptus.

Insulin-like growth factor II (IGF-II) gene expression was investigated in the early rat conceptus using in situ hybridisation. IGF-II mRNA has been detected as early as 7 days post coitum in the extraembryonic ectoderm of the egg cylinder (including the ectoplacental cone but excluding the trophoblast bordering the implantation chamber). There was no expression either in the early embryo at this stage or in the implanting blastocyst (5.5 days). At 9.5 days transcription was also detected in extra-embryonic mesodermal derivatives and the visceral yolk sac endoderm, but not in the embryonic region. At 10.5 days transcription was detected in embryonic mesodermal derivatives. High levels were found in the primitive heart, hepatic diverticulum and septum transversum; lower levels were found in the early somites and other primitive mesenchymal derivatives and midgut endoderm. No expression was detected at any stage in derivatives of the embryonic ectoderm, including the neurectoderm. Recent studies of IGF-II, the IGF-II/M-6-P receptor and enzymic extracellular matrix remodelling suggest that the expression of IGF-II in the early rat conceptus may be related to hyaluronate breakdown (with, or without, sulphated glycosaminoglycan synthesis), linked with the aggregation and differentiation of previously migrating mesenchymal cells.

Animals↗