Biomedical subjects

Z Li

Publications and source records attributed to Z Li.

At least 1,045 records · Page 58Linked to original sources

PubMed1997

Conservation of the centromere/kinetochore protein ZW10.

Mutations in the essential Drosophila melanogaster gene zw10 disrupt chromosome segregation, producing chromosomes that lag at the metaphase plate during anaphase of mitosis and both meiotic divisions. Recent evidence suggests that the product of this gene, DmZW10, acts at the kinetochore as part of a tension-sensing checkpoint at anaphase onset. DmZW10 displays an intriguing cell cycle-dependent intracellular distribution, apparently moving from the centromere/kinetochore at prometaphase to kinetochore microtubules at metaphase, and back to the centromere/kinetochore at anaphase (Williams, B.C., M. Gatti, and M.L. Goldberg. 1996. J. Cell Biol. 134:1127-1140). We have identified ZW10-related proteins from widely diverse species with divergent centromere structures, including several Drosophilids, Caenorhabditis elegans, Arabidopsis thaliana, Mus musculus, and humans. Antibodies against the human ZW10 protein display a cell cycle-dependent staining pattern in HeLa cells strikingly similar to that previously observed for DmZW10 in dividing Drosophila cells. Injections of C. elegans ZW10 antisense RNA phenocopies important aspects of the mutant phenotype in Drosophila: these include a strong decrease in brood size, suggesting defects in meiosis or germline mitosis, a high percentage of lethality among the embryos that are produced, and the appearance of chromatin bridges at anaphase. These results indicate that at least some aspects of the functional role of the ZW10 protein in ensuring proper chromosome segregation are conserved across large evolutionary distances.

Animals↗

PubMed1997

Infected macaques that controlled replication of SIVmac or nonpathogenic SHIV developed sterilizing resistance against pathogenic SHIV(KU-1).

Twenty macaques were used to evaluate the ability of nonpathogenic SIV(mac) or nonpathogenic chimeric SIV-HIV (SHIV) to induce protection in macaques against superinfection with a pathogenic variant of SHIV (SHIV(KU-1)) originally containing the tat, rev, vpu, and env of HIV-1 (strain HXB2) in a genetic background of SIV(mac)239. Specifically, three macaques inoculated with molecularly cloned, macrophage-tropic SIV(mac)LG1 developed an early systemic infection but recovered with only traces of SIV(mac) DNA in visceral lymphoid tissues. These animals were then inoculated parenterally with pathogenic SHIV(KU-1). All three animals resisted infection with SHIV(KU-1), as indicated by lack of virus recovery and absence of SHIV-specific env and vpu sequences in the visceral lymphoid tissues and multiple regions in the CNS. We also examined the ability of five macaques that had been inoculated with nonpathogenic SHIV (NP-SHIV) to withstand challenge with the pathogenic SHIV(KU-1). Like the SIV(mac)LG1-inoculated macaques, these animals also resisted SHIV(KU-1) challenge as judged by the inability to recover infectious virus, normal CD4+ T cell counts, and the absence of SHIV(KU-1) signature sequences in the lymph node tissue. Thus, eight of eight animals that developed control over primary lentivirus infections had also developed resistance to infection with pathogenic SHIV(KU-1). Three groups of macaques were used as controls for this study. The first group consisted of six macaques inoculated with SHIV(KU-1) alone. All animals developed viremia, showed severe loss of CD4+ T cells within 4 weeks, and succumbed to AIDS within 6 months. The second group of three macaques was inoculated first with SHIV(KU-1) and inoculated later with uncloned, neurovirulent SIV(mac)7F-Lu. A third group of three macaques was inoculated with SIV(mac)7F-Lu followed by inoculation with SHIV(KU-1). PCR analyses using oligonucleotide primers specific for the SIV or HIV env revealed that macaques from the last two groups had widespread infection with both SHIV(KU-1) and SIV(mac), indicating that animals that failed to control productive replication of either SHIV(KU-1) or SIV(mac)7F-Lu could not resist superinfection with the other virus. These data indicate that sterilizing immunity against the virulent SHIV could be induced in animals that had experienced an immunizing infection. Moreover, the divergence of the envelope glycoprotein of the protective avirulent and virulent challenge virus suggests that a single vaccine could protect against infection with a virus containing a different envelope glycoprotein.

Animals↗

PubMed1997

The traE gene of plasmid RP4 encodes a homologue of Escherichia coli DNA topoisomerase III.

The polypeptide encoded by the plasmid RP4 traE gene shows extensive protein sequence similarity to Escherichia coli topB, the gene encoding DNA topoisomerase III (Topo III). The traE gene product has been cloned into a bacteriophage T7-based transient expression system, and the polypeptide has been expressed and purified. The TraE protein exhibits topoisomerase activity similar to that of Topo III. Relaxation is stimulated by high temperature and low concentrations of Mg2+. In addition, similar to E. coli Topo III, the TraE protein is a potent decatenase and can substitute for Topo III activity in vivo. The biochemical properties of the TraE protein in vitro suggest that the protein may be involved in the resolution of plasmid DNA replication intermediates either during vegetative replication or in conjugative DNA transfer. Putative homologues of Topo III have been found to be encoded by other broad host range, conjugative plasmids isolated from both Gram-negative and Gram-positive organisms, suggesting that Topo III-like polypeptides may have an essential role in the propagation of many promiscuous plasmids.

Amino Acid Sequence↗

PubMed1997

Circularly permuted beta-lactamase from Staphylococcus aureus PC1.

The role that domain flexibility plays in the enzymatic activity of beta-lactamase from Staphylococcus aureus PC1 was investigated by producing two circularly permuted molecules. The C- and N-termini of the wild-type enzyme are adjacent to each other and remote from the active site, which is located between two domains. The polypeptide chain crosses over from one domain to the other twice. For the circularly permuted molecules, the termini were joined by an eight amino acid residue insertion, and new termini were introduced elsewhere. The first construct, termed cp254, was cleaved in a loop remote from the domain interface. The crystal structure of cp254 has been determined and refined at 1.8 A resolution, revealing essentially the same structure as that of the native protein. The activity profile with a representative sample of beta-lactam antibiotics is also very similar to that of wild-type beta-lactamase. The termini of the second circularly permuted mutant, cp228, occur within the second crossover region and therefore may enhance the flexibility of the molecule. Cp228 beta-lactamase shows a large decrease in enzymatic activity toward the sample of beta-lactam antibiotics, with catalytic rates that are 0.5-1% of those of the wild-type enzyme. One exception is the hydrolysis of the third generation cephalosporin, cefotaxime, which is hydrolyzed by the cp228 enzyme 10-fold faster than by wild-type beta-lactamase. Cp228 has not been crystallized. However, the circular dichroism spectra of the two circularly permuted proteins are very similar, indicating that, by analogy to cp254, cp228 adopts a global folded state. Thermal denaturation experiments reveal that cp254 is somewhat less stable than the wild-type enzyme, whereas cp228 is substantially less stable. Together, the data highlight the profound consequences that introducing flexibility at the domain interface has on both enzyme activity and protein stability.

Amino Acid Sequence↗

PubMed1997

Cloning of a novel T-cell protein FYB that binds FYN and SH2-domain-containing leukocyte protein 76 and modulates interleukin 2 production.

T cell receptor zeta (TcRzeta)/CD3 ligation initiates a signaling cascade that involves src kinases p56(lck) and zeta-associated protein 70, leading to the phosphorylation of substrates such as TcRzeta, Vav, SH2-domain-containing leukocyte protein 76 (SLP-76), cbl, and p120/130. FYN binding protein (FYB or p120/130) associates with p59(fyn), the TcRzeta/CD3 complex, and becomes tyrosine-phosphorylated in response to receptor ligation. In this study, we report the cDNA cloning of human and murine FYB and show that it is restricted in expression to T cells and myeloid cells and possesses an overall unique hydrophilic sequence with several tyrosine-based motifs, proline-based type I and type II SH3 domain binding motifs, several putative lysine/glutamic acid-rich nuclear localization motifs, and a SH3-like domain. In addition to binding the src kinase p59(fyn), FYB binds specifically to the hematopoietic signaling protein SLP-76, an interaction mediated by the SLP-76 SH2 domain. In keeping with this, expression of FYB augmented interleukin 2 secretion from a T cell hybridoma, DC27.10, in response to TcRzeta/CD3 ligation. FYB is therefore a novel hematopoietic protein that acts as a component of the FYN and SLP-76 signaling cascades in T cells.

Adaptor Proteins, Signal Transducing↗

PubMed1997

The prostacyclin analogue carbacyclin inhibits Ca(2+)-activated K+ current in aortic baroreceptor neurones of rats.

1. Previous studies indicate that prostacyclin (PGI2) increases the activity of baroreceptor afferent fibres. The purpose of this study was to test the hypothesis that PGI2 inhibits Ca(2+)-activated K+ current (IK(Ca))in isolated baroreceptor neurones in culture. 2. Rat aortic baroreceptor neurones in the nodose ganglia were labelled in vivo by applying a fluorescent dye (DiI) to the aortic arch 1-2 weeks before dissociation of the neurones. Outward K+ currents in baroreceptor neurones evoked by depolarizing voltage steps from a holding potential of -40 mV were recorded using the whole-cell patch-clamp technique. 3. Exposure of baroreceptor neurones to the stable PGI2 analogue carbacyclin significantly inhibited the steady-state K+ current in a dose-dependent and reversible manner. The inhibition of K+ current was not caused indirectly by changes in cytosolic Ca2+ concentration. The Ca(2+)-activated K+ channel blocker charybdotoxin (ChTX, 10(-7) M) also inhibited the K+ current. In the presence of ChTX or in the absence of Ca2+, carbacyclin failed to inhibit the residual K+ current. Furthermore, in the presence of high concentrations of carbacyclin, ChTX did not cause further reduction of K+ current. 4. Carbacyclin-induced inhibition of IK(Ca) was mimicked by 8-bromo-cAMP and by activation of G-protein with GTP gamma S. The inhibitory effect of carbacyclin on IK(Ca) was abolished by GDP beta S, which blocks G-protein activation, and by a selective inhibitor of cAMP-dependent protein kinase, PKI5-24. 5. The results demonstrate that carbacyclin inhibits ChTX-sensitive IK(Ca) in isolated aortic baroreceptor neurones by a G-protein-coupled activation of cAMP-dependent protein kinase. This mechanism may contribute to the PGI2-induced increase in baroreceptor activity demonstrated previously.

Animals↗

PubMed1997

Characterization of the pathogenic KU-SHIV model of acquired immunodeficiency syndrome in macaques.

By animal-to-animal passage in macaques we derived a pathogenic chimeric simian-human immunodeficiency virus (SHIV) that caused CD4+ T cell loss and AIDS in pigtail macaques and used it to inoculate 20 rhesus and pigtail macaques by the intravaginal and intravenous routes. On the basis of the outcome of infection and patterns of CD4+ T cell loss and viral load, disease was classified into four patterns: acute, subacute, chronic, and nonprogressive infection. During the study period, 15 of the 20 animals developed fatal disease, including AIDS, encephalitis, pneumonia, and severe anemia. Opportunistic pathogens identified in these animals included Pneumocystis, cytomegalovirus, Cryptosporidium, Toxoplasma, and Candida. No single parameter by itself predicted outcome, although a combination of low CD4+ T cell counts in blood, high plasma virus levels, and presence of autoantibodies to red blood cells reliably predicted a fatal outcome. Five animals (25%) died within 3 months of inoculation and constituted the group with acute disease, whereas the nine animals (45%) with subacute disease died between 3 and 8 months postinoculation. This 70% mortality within 8 months is significantly shorter than in HIV-1-infected human beings, of whom 70% develop fatal disease a decade after infection. SHIV infection in macaques provides a useful model with which to evaluate antiviral strategies, combining all the advantages of the SIVmac system, yet using a virus bearing the envelope gene of HIV-1.

AIDS-Related Opportunistic Infections↗

PubMed1997

A recombinant adenovirus expressing p27Kip1 induces cell cycle arrest and loss of cyclin-Cdk activity in human breast cancer cells.

In order to elucidate the biochemical mechanisms by which the universal cyclin kinase inhibitor p27Kip1 regulates cell cycle progression in human breast cancer cells, a recombinant adenovirus expressing human p27 was constructed (Adp27). Upon infection of human breast cancer cells MDA-MB-231 and MCF-7 with Adp27, a high level of p27 expression was observed, and this resulted in a marked decrease in the proportion of cells in S-phase. In multiple cell lines, comparison of the cytotoxicity of Adp27 with another adenovirus vector expressing the related universal cyclin kinase inhibitor WAF1/Cip1 (AdWAF1), showed Adp27 to be markedly more (up to 56-fold) toxic than AdWAF1. DNA histograms showed Adp27 to cause a G1/S arrest at lower viral doses than AdWAF1. Analysis of cyclin dependent kinase activity following Adp27 infections showed decreased Cdk2 and cyclin B1-Cdc2 activity at lower viral doses when compared with AdWAF1. Adp27 is therefore potentially useful for studies of growth regulation and for gene therapy when growth inhibition is desired.

Adenoviridae↗

PubMed1997

A cell-free stock of simian-human immunodeficiency virus that causes AIDS in pig-tailed macaques has a limited number of amino acid substitutions in both SIVmac and HIV-1 regions of the genome and has offered cytotropism.

We have examined both the sequence changes in the LTR, gag, vif, vpr, vpx, tat, rev, vpu, env, and nef genes and the cell tropism of a cell-free stock of chimeric simian-human immunodeficiency virus (SHIV) isolated from the cerebrospinal fluid of a pig-tailed macaque (PNb) that developed AIDS. This virus (SHIVKU-1) is highly pathogenic when inoculated into other macaques. DNA sequence analysis of PCR-amplified products revealed a total of 5 nucleotide changes in the LTR while vif had 2 consensus amino acid changes. The gag, vif, and vpx had no consensus amino acid substitutions, whereas vpr had 1 consensus substitution. The tat and rev genes of the HXB2 region of SHIVKU-1 had 2 and 1 consensus amino acid changes, respectively. The vpu gene of the HXB2 region of SHIV, which originally had an ACG at the beginning of the gene, reverted to an initiation ATG codon and in addition contained a consensus amino acid substitution at position 69 of this protein. As expected, the majority of the nucleotide substitutions were found in the env and nef genes. Thirteen and 5 amino acid changes were predicted for the corresponding Env and Nef proteins, respectively. In addition, one-third of the env gene clones isolated from the SHIVKU-1 stock had a 5-amino-acid deletion in the V4 region. Using three independent assays, we determined that the changes in the SHIVKU-1 were associated with an increase in the efficiency of replication in macrophages. The strikingly few consensus changes in the virus suggest that conversion of this virus to one capable of causing AIDS in pig-tailed macaques was associated with relatively few changes in the viral envelope and/or accessory genes. These results will provide the basis for the development of a pathogenic, molecular clone of SHIV capable of causing AIDS in pig-tailed macaques.

Acquired Immunodeficiency Syndrome↗

PubMed1997

Structure-function studies of p38 mitogen-activated protein kinase. Loop 12 influences substrate specificity and autophosphorylation, but not upstream kinase selection.

Several mitogen-activated protein kinase (MAPK) cascades have been identified in eukaryotic cells. The activation of MAPKs is carried out by distinct MAPK kinases (MEKs or MKKs), and individual MAPKs have different substrate preferences. Here we have examined how amino acid sequences encompassing the dual phosphorylation motif located in the loop 12 linker (L12) between kinase subdomains VII and VIII and the length and amino acid sequence of L12 influence autophosphorylation, substrate specificity, and upstream kinase selectivity for the MAPK p38. Conversion of L12 of p38 to an "ERK-like" structure was accomplished in several ways: (i) by replacing glycine with glutamate in the dual phosphorylation site, (ii) by placing a six-amino acid sequence present in L12 of ERK (but absent in p38) into p38, and (iii) by mutations of amino acid residues in loop 12. Two predominant effects were noted: (i) the Xaa residue in the dual phosphorylation motif Thr-Xaa-Tyr as well as the length of L12 influence p38 substrate specificity, and (ii) the length of L12 plays a major role in controlling autophosphorylation. In contrast, these modifications do not result in any change in the selection of p38 by individual MAPK kinases.

Amino Acid Sequence↗

PubMed1997

Differential expression of proteins regulating cell cycle progression in growth vs. differentiation.

The level of various G1 cyclins and cyclin-dependent kinases (cdks) present in the nuclei of synchronized ML-1 human myeloblastic leukemia cells was determined as a function of time after initiation of cell growth with insulin-like growth factor-1 (IGF-1) and transferrin (Tf), and following induction of differentiation with transforming growth factor-beta1 (TGF-beta1). Cyclin E and cdk2 were expressed at relatively high levels in the nuclei of proliferation-stimulated cells, whereas cyclin D1 and cdk5 were expressed at comparably high levels in the nuclei of differentiation-induced cells. In the nuclear extracts from proliferation-stimulated cells, cyclin E complexed specifically with cdk2, whereas in nuclear extracts from differentiation-induced cells, cyclin D1 bound specifically to cdk5. Increased cyclin E/cdk2 expression was accompanied by increased DNA synthesis, whereas increased cyclin D1/cdk5 levels correlated with decreased DNA synthesis. In both growth- and differentiation-induced cells, cyclin D2 expression preceded the expression of cyclin D3, and a significantly larger amount of these cyclins was present in differentiation- as compared to proliferation-induced cells. In contrast, cdk4 and cdk6 were present at similar levels in the nuclear extracts from both growth- and differentiation-induced cells. These data show that, in ML-1 cells, the proliferation-associated progression from G1 to S, as well as the differentiation-associated transit from G1 to maturation is accompanied by the expression of specific cyclin/cdk pairs, comprising cdk2/cyclin E in growth and cdk5/cyclin D1 in differentiation.

CDC2-CDC28 Kinases↗

PubMed1997

Activation of the transcription factor MEF2C by the MAP kinase p38 in inflammation.

For cells of the innate immune system to mount a host defence response to infection, they must recognize products of microbial pathogens such as lipopolysaccharide (LPS), the endotoxin secreted by Gram-negative bacteria. These cellular responses require intracellular signalling pathways, such as the four MAP kinase (MAPK) pathways. In mammalian cells the MAPK p38 is thought to play an important role in the regulation of cellular responses during infection through its effects on the expression of proinflammatory molecules. One means of understanding the role of p38 in these responses is to identify proteins with functions regulated by p38-catalysed phosphorylation. Here we demonstrate a link between the p38 pathway and a member of the myocyte-enhancer factor 2 (MEF2) group of transcription factors. We found that in monocytic cells, LPS increases the transactivation activity of MEF2C through p38-catalysed phosphorylation. One consequence of MEF2C activation is increased c-jun gene transcription. Our results show that p38 may influence host defence and inflammation by maintaining the balance of c-Jun protein consumed during infection.

Binding Sites↗

PubMed1997

Surface and peripheral doses of dynamic and physical wedges.

PURPOSE: The physical and dosimetric differences between three different wedge systems on a multileaf collimator (MLC) equiped linear accelerator are discussed in this report. In particular, the in-field and peripheral surface doses from these wedge systems are measured and their clinical differences discussed. METHODS AND MATERIALS: A parallel-plate chamber was used in a solid water phantom to measure the surface doses of the wedges. Published correction factors were used to convert relative ionization to relative surface dose. Measurements were performed for 6 and 18 MV photon beams for different field sizes, source-surface distances (SSD), and distances outside the field for peripheral dose measurements. Surface-dose profiles across a field in the wedge-gradient direction were measured for the dynamic and upper wedges. Dose profiles in the nonwedge gradient direction were measured for open beam as well as the three wedges using films at depths of maximum dose (d(max)). RESULTS: At 85 cm SSD, surface doses on the central axis under a dynamic wedge or upper wedges are similar to those of an open field, while those of a lower wedged field are as much as 100% higher. Differences in surface doses due to beam energy are relatively minor compared with differences due to SSD or wedge systems. Dynamic and upper wedges produce similar peripheral doses, much lower than those produced by the lower wedges. The surface dose profile across the field under the dynamic wedge has a higher slope than that under the upper wedge, when the difference in wedge angles is compensated for by normalization to the dose profile at d(max). In the nonwedge gradient direction, the dose profiles at d(max) of both the upper and the lower wedges demonstrate a marked effect of oblique filtration of the primary beam, resulting in an off-axis ratio at 80% of the field width of 0.95, in contrast to the off-axis ratio of 1.05 in the open and the dynamic wedged fields. CONCLUSIONS: The three wedge systems produce significantly different surface and peripheral doses that should be considered in properly choosing a wedge system for clinical use. Dynamic wedge and upper wedge systems deliver surface and peripheral doses similar to those of open fields and much lower than the lower wedge system. Both physical wedge systems degrade beam profiles in the nonwedged direction.

Equipment Design↗

PubMed1997

Early treatment with 9-(2-phosphonylmethoxyethyl)adenine reduces virus burdens for a prolonged period in SIV-infected rhesus macaques.

We evaluated the effects of a reverse transcriptase inhibitor, 9-(2-phosphonylmethoxyethyl)adenine (PMEA), on simian immunodeficiency virus (SIV) infection in rhesus macaques (Macaca mulatta). Four macaques were given PMEA (20 mg/kg) subcutaneously on days 1 and 2 and inoculated with virus on day 2. Drug treatment was continued for 30 consecutive days, after which the virus burdens and course of infection were monitored for a further 6 months. Four control animals that did not receive PMEA all developed high virus burdens and two of the four developed clinical disease. In contrast, virus burdens remained low in three of the four macaques treated with PMEA and all four remained healthy. Our results show that suppression of virus replication early in infection can result in reduced virus burdens for a much longer period.

Adenine↗

PubMed1997

Purification, cDNA sequence, and tissue distribution of rat uroguanylin.

Guanylin, a peptide purified from rat jejunum, is thought to regulate water and electrolyte balance in the intestine. We show here, using a combination of Northern blots, Western blots, and functional assays, that guanylin and its receptor (GCC) are not distributed in parallel within the rat intestine. To investigate the possibility that there might be a second intestinal peptide that serves as a ligand for GCC, we assayed tissue extracts for the ability to stimulate cyclic GMP synthesis in a GCC-expression cell line. Duodenal extracts display a peak of biological activity that is not present in colon and that does not comigrate with guanylin or proguanylin. The activity co-purifies with a novel peptide (TIATDECELCINVACTGC) that has high homology with uroguanylin, a peptide initially purified from human and opossum urine. A rat uroguanylin cDNA clone was found to encode a propeptide whose C-terminus corresponds to our purified peptide. Northern blots with probes generated from this clone reveal that prouroguanylin mRNA is strongly expressed in proximal small intestine, but virtually absent from colon, corroborating our biochemical measurements. Taken together, these studies demonstrate an intestinal origin for uroguanylin, and show that within the intestine its distribution is complementary to that of guanylin.

Amino Acid Sequence↗

PubMed1997

Ca2+ release from internal stores: role in generating depolarizing after-potentials in rat supraoptic neurones.

1. Influences of Ca2+ release from internal stores on the generation of depolarizing after-potentials (DAPs) were investigated in magnocellular neurones of rat supraoptic nucleus (SON) using whole-cell patch recording techniques in brain slices. 2. DAPs were recorded from more than half of the cells encountered, and following evoked single spikes had an amplitude of 3.00 +/- 0.19 mV (mean +/- S.E.M.) and lasted for 1.02 +/- 0.06 s. Their sizes usually increased with the number of preceding spikes, but could be reduced or eliminated when intervals between consecutive current pulses evoking tens of spikes were short. 3. DAPs were eliminated by removal of external Ca2+, and significantly reduced by bath application of nifedipine or omega-conotoxin. 4. Blockade of Ca2+ release from internal stores by perifusion with ryanodine or dantrolene, or direct diffusion of Ruthenium Red into cells suppressed DAP amplitudes by approximately 50% and shortened their durations. 5. Depletion of internal Ca2+ stores by perifusion with thapsigargin or cyclopiazonic acid also reduced DAP amplitudes by approximately 50% and eliminated phasic patterns of firing. 6. Caffeine, an agent known to enhance intracellular Ca2+ release, amplified DAPs and promoted phasic firing. 7. These results suggest that Ca2+ influx via high-voltage-activated Ca2+ channels in SON cells triggers ryanodine receptor-mediated Ca2+ release from internal stores. This process enhances DAPs and promotes phasic firing in SON cells, and would thus contribute to vasopressin release.

Animals↗

PubMed1997

Structure and transcription of the gene for translation elongation factor 1 subunit alpha of zebrafish (Danio rerio).

The zebrafish gene for translation elongation factor 1 alpha (EF1 alpha) was isolated from a phage Lambda genomic library and sequence and structure determined. One gene copy of EF1 alpha per haploid set of chromosomes was found and no processed pseudogenes. A highly active promoter region was localized to a 277 bp PstI/PvuII fragment beginning 240 bp upstream from the tsp, but no transcription enhancing, or silencing activity was observed within 1 kbp upstream, or downstream from the promoter. Expression of EF1 alpha appears to be developmentally regulated.

Animals↗

PubMed1997

Heritability of plasma leptin in a population sample of African-American families.

The aim of this study was to examine familial patterns of plasma leptin levels and the potential association with cardiovascular risk factors in a population sample of African-American families recruited from metropolitan Chicago. The study included 68 mothers, 31 fathers, 143 daughters, and 119 sons, for a total of 361 individuals from 118 families. Leptin levels were adjusted for the effect of age separately for mothers, fathers, daughters, and sons. Residuals were then standardized before estimating familial correlation using the maximum-likelihood method available in SEGPATH. With the exception of height, plasma leptin level was strongly correlated with all measured anthropometric variables. Familial effect (i.e., heritability) of leptin levels was estimated as 39% in this population at high risk for over weight. A significant sex difference was observed, and most of the estimated familial effect may be attributed to genetic influences since the spouse correlation was not statistically different from zero. A strong nonshared environmental effect is also suggested, however.

Anthropometry↗