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At least 1,783 records · Page 99Linked to original sources
PubMed2003

Rho3p regulates cell separation by modulating exocyst function in Schizosaccharomyces pombe.

Cytokinesis is the final stage of the cell division cycle in which the mother cell is physically divided into two daughters. In recent years the fission yeast Schizosaccharomyces pombe has emerged as an attractive model organism for the study of cytokinesis, since it divides using an actomyosin ring whose constriction is coordinated with the centripetal deposition of new membranes and a division septum. The final step of cytokinesis in S. pombe requires the digestion of the primary septum to liberate two daughters. We have previously shown that the multiprotein exocyst complex is essential for this process. Here we report the isolation of rho3(+), encoding a Rho family GTPase, as a high-copy suppressor of an exocyst mutant, sec8-1. Overproduction of Rho3p also suppressed the temperature-sensitive growth phenotype observed in cells lacking Exo70p, another conserved component of the S. pombe exocyst complex. Cells deleted for rho3 arrest at higher growth temperatures with two or more nuclei and uncleaved division septa between pairs of nuclei. rho3Delta cells accumulate approximately 100-nm vesicle-like structures. These phenotypes are all similar to those observed in exocyst component mutants, consistent with a role for Rho3p in modulation of exocyst function. Taken together, our results suggest the possibility that S. pombe Rho3p regulates cell separation by modulation of exocyst function.

Actins↗
PubMed1993

Generation of band-specific painting probes from a single microdissected chromosome.

We have developed a modified strategy for the generation of regional probes for human chromosomes by microdissection and degenerate oligonucleotide primed PCR. This modification dramatically increases the efficiency of amplification by pretreatment of the dissected chromatin with topoisomerase I (Topo I) before PCR. This protocol has enabled us to construct region-specific probes for fluorescence in situ hybridization (FISH) from a single microdissected chromosome. Results are presented which convincingly demonstrate that this new method generates high intensity region-specific FISH probes, while at the same time significantly decreasing the time-consuming and labor-intensive aspects of microdissection. The reduction of the number of copies required to generate a useful probe also significantly decreases the risk of contamination during the microdissection process. We believe this advance will allow microdissection to be more widely used in the cytogenetic analysis of chromosome rearrangements in both cancer and hereditary diseases. In addition, this method now makes it possible to construct a series of non-overlapping band-specific DNA microclone libraries to provide complete coverage of individual chromosomes for physical mapping.

Base Sequence↗
PubMed1985

Apparent generation of a segmented mRNA from two separate tandem gene families in Trypanosoma cruzi.

Using a cDNA for an abundant Trypanosoma cruzi mRNA as probe, we have cloned and sequenced a gene which is organized in at least 20 nearly perfect tandem repeats of 940 base pairs. The 5' end of the mRNA has been sequenced by primer extension and found to contain a 35 nucleotide mini-exon (or spliced-leader) sequence that is ubiquitous in trypanosome mRNAs. This sequence, however, is not present in the tandem genomic repeats which encode the exon containing the major portion of the mRNA. Previous studies have shown that the 35-nucleotide sequence is encoded by a separate tandem gene family. One model to explain the formation of a segmented mRNA invokes priming of transcription by a small RNA which contains the leader sequence at its 5' end. However, northern blot analysis of total trypanosome RNA reveals a ladder of molecules larger than the mature mRNA, which appear to be faithful multimeric copies of the tandem gene. The discrete sizes of these RNAs correspond to those expected for partially processed precursors. These observations lend credence to the possibility of an alternative model where segmented mRNAs are generated by inter-molecular splicing.

Animals↗
PubMed1992

Intron requirement for expression of the human purine nucleoside phosphorylase gene.

Abbreviated purine nucleoside phosphorylase (PNP) genes were engineered to determine the effect of introns on human PNP gene expression. PNP minigenes containing the first intron (complete or shortened from 2.9 kb down to 855 bp), the first two introns or all five PNP introns resulted in substantial human PNP isozyme expression after transient transfection of murine NIH 3T3 cells. Low level human PNP activity was observed after transfection with a PNP minigene containing the last three introns. An intronless PNP minigene construct containing the PNP cDNA fused to genomic flanking sequences resulted in undetectable human PNP activity. Heterogeneous, stable NIH 3T3 transfectants of intron-containing PNP minigenes (verified by Southern analysis), expressed high levels of PNP activity and contained appropriately processed 1.7 kb message visualized by northern analysis. Stable transfectants of the intronless PNP minigene (40-45 copies per haploid genome) contained no detectable human PNP isozyme or mRNA. Insertion of the 855 bp shortened intron 1 sequence in either orientation upstream or downstream of a chimeric PNP promoter-bacterial chloramphenicol acetyltransferase (CAT) gene resulted in a several-fold increase in CAT expression in comparison with the parental PNP-CAT construct. We conclude that human PNP gene expression at the mRNA and protein level is dependent on the presence of intronic sequences and that the level of PNP expression varies directly with the number of introns included. The disproportionately greatest effect of intron 1 can be explained by the presence of an enhancer-like element retained in the shortened 855 bp intron 1 sequence.

3T3 Cells↗
PubMed2001

Digging for dead genes: an analysis of the characteristics of the pseudogene population in the Caenorhabditis elegans genome.

Pseudogenes are non-functioning copies of genes in genomic DNA, which may either result from reverse transcription from an mRNA transcript (processed pseudogenes) or from gene duplication and subsequent disablement (non-processed pseudogenes). As pseudogenes are apparently 'dead', they usually have a variety of obvious disablements (e.g., insertions, deletions, frameshifts and truncations) relative to their functioning homologs. We have derived an initial estimate of the size, distribution and characteristics of the pseudogene population in the Caenorhabditis elegans genome, performing a survey in 'molecular archaeology'. Corresponding to the 18 576 annotated proteins in the worm (i.e., in Wormpep18), we have found an estimated total of 2168 pseudogenes, about one for every eight genes. Few of these appear to be processed. Details of our pseudogene assignments are available from http://bioinfo.mbb.yale.edu/genome/worm/pseudogene. The population of pseudogenes differs significantly from that of genes in a number of respects: (i) pseudogenes are distributed unevenly across the genome relative to genes, with a disproportionate number on chromosome IV; (ii) the density of pseudogenes is higher on the arms of the chromosomes; (iii) the amino acid composition of pseudogenes is midway between that of genes and (translations of) random intergenic DNA, with enrichment of Phe, Ile, Leu and Lys, and depletion of Asp, Ala, Glu and Gly relative to the worm proteome; and (iv) the most common protein folds and families differ somewhat between genes and pseudogenes-whereas the most common fold found in the worm proteome is the immunoglobulin fold and the most common 'pseudofold' is the C-type lectin. In addition, the size of a gene family bears little overall relationship to the size of its corresponding pseudogene complement, indicating a highly dynamic genome. There are in fact a number of families associated with large populations of pseudogenes. For example, one family of seven-transmembrane receptors (represented by gene B0334.7) has one pseudogene for every four genes, and another uncharacterized family (represented by gene B0403.1) is approximately two-thirds pseudogenic. Furthermore, over a hundred apparent pseudogenic fragments do not have any obvious homologs in the worm.

Amino Acid Sequence↗
PubMed1997

Structural and evolutionary studies on sterol 14-demethylase P450 (CYP51), the most conserved P450 monooxygenase: I. Structural analyses of the gene and multiple sizes of mRNA.

The structure of rat CYP51 gene encoding sterol 14-demethylase was examined. The CYP51 gene spanned about 18 kb and contained 10 exons. The copy number of CYP51 in the rat genome was determined to be one. In addition, one CYP51 processed (intron-less) pseudogene covering the coding and ca. 600-bp 3'-noncoding sequences of CYP51 cDNA was found in the rat genome. Multiple transcription initiation sites were predicted by primer extension and 5'-RACE methods using poly(A)+ RNA from liver, ovary, and testis, and the major ones were located at 126 and 123 nucleotides upstream from the initiation ATG codon. The primer extension also showed several minor sites around the major ones. In addition to these sites, other minor initiation sites were also predicted at around 330 and 460 nucleotides upstream from the initiation ATG codon. No TATA box was found in the putative promoter region, but multiple GC boxes were found around the cap sites, supporting the previously inferred housekeeping nature of CYP51 gene and the existence of the multiple transcription initiation sites. A few consensus transcription regulatory elements such as CRE were found in the 5'-flanking region. Four polyadenylation signals were found in the 3'-noncoding region by the 3'-RACE method. Three of them were used to generate 3.1-, 2.7-, and 2.3-kb mRNAs in liver and ovary. The remaining one was used only in testis to generate 1.9-kb mRNA having an unusually short trailer sequence, suggesting a specific regulatory mechanism for generating CYP51 mRNA in testis different from that in liver and ovary.

Amino Acid Sequence↗
PubMed1993

Transgenetic investigations of prion diseases of humans and animals.

Prions cause transmissible and genetic neurodegenerative diseases. Infectious prion particles are composed largely, if not entirely, of an abnormal isoform of the prion protein (PrPSc), which is encoded by a chromosomal gene. Although the PrP gene is single copy, transgenic mice with both alleles of the PrP gene ablated develop normally. A post-translational process, as yet unidentified, converts the cellular prion protein (PrPC) into PrPSc. Scrapie incubation times, neuropathology and prion synthesis in transgenic mice are controlled by the PrP gene. Mutations in the PrP gene are genetically linked to development of neurodegeneration. Transgenic mice expressing mutant PrP spontaneously develop neurological dysfunction and spongiform neuropathology. Investigations of prion diseases using transgenesis promise to yield much new information about these once enigmatic disorders.

Animals↗
PubMed2003

Shuffling of genes within low-copy repeats on 22q11 (LCR22) by Alu-mediated recombination events during evolution.

Low-copy repeats, or segmental duplications, are highly dynamic regions in the genome. The low-copy repeats on chromosome 22q11.2 (LCR22) are a complex mosaic of genes and pseudogenes formed by duplication processes; they mediate chromosome rearrangements associated with velo-cardio-facial syndrome/DiGeorge syndrome, der(22) syndrome, and cat-eye syndrome. The ability to trace the substrates and products of recombination events provides a unique opportunity to identify the mechanisms responsible for shaping LCR22s. We examined the genomic sequence of known LCR22 genes and their duplicated derivatives. We found Alu (SINE) elements at the breakpoints in the substrates and at the junctions in the truncated products of recombination for USP18, GGT, and GGTLA, consistent with Alu-mediated unequal crossing-over events. In addition, we were able to trace a likely interchromosomal Alu-mediated fusion between IGSF3 on 1p13.1 and GGT on 22q11.2. Breakpoints occurred inside Alu elements as well as in the 5' or 3' ends of them. A possible stimulus for the 5' or 3' terminal rearrangements may be the high sequence similarities between different Alu elements, combined with a potential recombinogenic role of retrotransposon target-site duplications flanking the Alu element, containing potentially kinkable DNA sites. Such sites may represent focal points for recombination. Thus, genome shuffling by Alu-mediated rearrangements has contributed to genome architecture during primate evolution.

Alu Elements↗
PubMed1989

Dynamical neural network organization of the visual pursuit system.

The central nervous system is a parallel dynamical system which connects sensory input with motor output for the performance of visual tracking. This paper applies elementary control system tools to extend dynamical neural network models to the visual smooth pursuit system. Observed eye position responses to target motions and characteristics of the plant (eye muscles and orbital mechanics) place dynamical constraints on the interposed neural network controller. In the process of constructing a model for the controller, we show two previous pursuit system models, using efference copy and feedforward compensation, are equivalent from an input-output standpoint. We introduce a controller model possessing a potentially highly parallel implementation and offer an example with supporting neural firing rate data. Changes in time delays or other system dynamics are expected to lead to compensatory adaptive changes in the controller. A scheme to noninvasively simulate such changes in system dynamics was developed. Actual physiologic data of adaptive responses to increased time delay is presented as an example of the utility of this parallel controller. Compensatory changes in our parallel controller model are easily predicted. These results suggest a productive interaction between neural network modeling, neurophysiology, and control systems engineering.

Animals↗
PubMed1995

Characterization of two distinct calcium-binding sites in the amino-terminus of human profilaggrin.

Profilaggrin is a large phosphorylated protein (approximately 400 kDa in humans) that is expressed in the granular cells of epidermis where it forms a major component of keratohyalin. It consists of multiple copies of similar filaggrin units plus amino- and carboxy-terminal domains that differ from filaggrin. Proteolytic processing of profilaggrin during terminal differentiation results in the removal of these domains and generation of monomeric filaggrin units, which associate with keratin intermediate filaments to form macrofibrils in the stratum corneum. The amino-terminal domain contains two calcium-binding motifs similar to the EF-hands found in the S-100 family of calcium-binding proteins. In this report, we expressed the 293-residue amino-terminal pro-domain of human profilaggrin as a polyhistidine fusion protein in Escherichia coli, and characterized calcium binding by a 45Ca++ binding assay and fluorescence emission spectroscopy. Fluorescence measurements indicated that the profilaggrin polypeptide undergoes conformational changes upon the removal of Ca++ with ethylenediamine tetraacetic acid, demonstrating the presence of two calcium-binding sites with affinities for calcium that differ ninefold (1.4 x 10(-4) M and 1.2 x 10(-3) M). We suggest that this functional calcium-binding domain at the amino-terminus of human profilaggrin plays a role in profilaggrin processing and in other calcium-dependent processes during terminal differentiation of the epidermis.

Amino Acid Sequence↗
PubMed1993

The partition (par) locus of pSC101 is an enhancer of plasmid incompatibility.

The incompatibility that pSC101-derived plasmids express toward each other is mediated by directly repeated sequences (iterons) located near the plasmid's replication origin. We report here that the pSC101 par locus, which stabilizes plasmid inheritance in dividing cell populations and alters DNA superhelicity, can function as a cis-acting enhancer of incompatibility, which we show is determined jointly by the copy number of the plasmid and the number of iterons per copy. A single synthetic 32 bp iteron sequence carried by the pUC19 plasmid confers strong pSC101-specific incompatibility in the absence of any other pSC101 sites but requires the par locus to express strong incompatibility when carried by a lower-copy-number plasmid. We propose a model by which the par locus can enhance the apparently antagonistic processes of incompatibility and pSC101 DNA replication while concurrently facilitating plasmid distribution during cell division.

Bacterial Proteins↗
PubMedDate not supplied

Transkinetoplastidy--a novel phenomenon involving bulk alterations of mitochondrion-kinetoplast DNA of a trypanosomatid protozoan.

Dramatic and consistent changes of mitochondria or kinetoplast DNA (kDNA) were observed in certain variants of Leishmania amazonensis (A variants) selected in vitro for arsenite-resistance. This was found initially by comparing different lots of wild-type cells and their respective A variants resistant to 30 microM arsenite. The kDNAs isolated from these two groups had different restriction patterns and hybridized poorly to each other, whereas those from different lots within each of the two groups were identical. Hybridization data showed an overall identity of less than 10(-3) between total kDNAs of the two groups. This difference was further examined in three independent series of variants, which were selected from three different clones for resistance to graded concentrations of arsenite (5-50 microM). In all three series, their kDNAs were found to change abruptly in an identical pattern at a late step of the selection process, i.e., A variants resistant to 15 microM or 30 microM arsenite. There was no apparent loss of kDNA in the process. Most of the changes observed appear to involve a shift in either the dominance or the copy number of different minicircle subclasses. Surprisingly, the kDNAs of tunicamycin-resistant variants (T variants) were also found to undergo similar changes. Genetic changes previously described in both A and T variants are limited to their nuclei. Namely, different chromosomal regions are amplified to produce large DNA circles which are responsible for the drug-resistant phenotypes. Interestingly, other arsenite-resistant clones without such chromosomal DNA amplification (A' variants) had kDNA of the wild-type pattern. The profound changes of kDNA observed are unprecedented. We propose the term "transkinetoplastidy" for this phenomenon to distinguish it from dyskinetoplastidy or the loss of kDNA described previously in trypanosomatid protozoa. This phenomenon is discussed with respect to the possible mechanisms of its generation, regulation and relation to the drug-resistant phenotypes.

Animals↗
PubMed1998

Cloning and characterization of the phenylalanyl-tRNA synthetase beta subunit gene from Candida albicans.

A Candida albicans expression library was constructed from RNA isolated from regenerating protoplasts. A 1.4-kb cDNA clone was used to isolate a genomic fragment. Sequence analysis revealed an open reading frame of 593 amino acids with an overall identity of 63.6% with the phenylalanyl-tRNA synthetase beta subunit (FRS1) of Saccharomyces cerevisiae. We named it CaFRS1. It is located in a single copy in chromosome R, SfiI fragment M. Its expression showed a decrease during the cell wall regeneration process in protoplasts of both yeast and mycelial cells of C. albicans, suggesting its requirement thereof in initial steps of the cell wall synthesis.

Amino Acid Sequence↗
PubMed1998

IS195, an insertion sequence-like element associated with protease genes in Porphyromonas gingivalis.

Porphyromonas gingivalis is recognized as an important etiologic agent in adult and early-onset periodontal disease. Proteases produced by this organism contribute to its virulence in mice. Protease-encoding genes have been shown to contain multiple copies of repeated nucleotide sequences. These conserved sequences have also been found in hemagglutinin genes. In the process of studying the genetic loci containing the conserved repeated sequences, we have characterized a prtP gene homolog from P. gingivalis W83 encoding a cysteine protease with Lys-X specificity. However, this prtP gene was interrupted by an insertion sequence-like element which we designated IS195. Furthermore, IS195 and another element, IS1126, were present downstream of prtP gene homologs (kgp) found in P. gingivalis H66 and 381. IS195, a 1,068-bp insertion sequence-like element, contained 11-bp inverted repeats at its termini and was bordered by 9-bp direct repeats presumed to be a transposition-mediated target site duplication. Its central region contained one large open reading frame encoding a predicted 300-amino-acid protein which appeared to be a transposase. We isolated two naturally occurring variants of P. gingivalis W83, one carrying IS195 within the coding region of the prtP gene and another containing an intact prtP gene. Biochemical characterization revealed a lack of trypsin-like Lys-X specific proteolytic activity in the P. gingivalis W83 variant carrying the disrupted prtP gene. Studies using a mouse model revealed a reduction of virulence resulting from insertion of IS195 into the coding region of the prtP gene. An allelic-exchange mutant defective in the prtP gene also was constructed and tested in vivo. It displayed intermediate virulence compared to that of the wild-type and prtP::IS195 mutant strains. We conclude that the Lys-X cysteine protease contributes to virulence in soft tissue infections.

Amino Acid Sequence↗
PubMed1996

The cryptic general secretory pathway (gsp) operon of Escherichia coli K-12 encodes functional proteins.

Systematic sequencing of the Escherichia coli K-12 chromosome (GenBank entry U18997) has revealed the presence of an apparently complete operon of genes (the gspC-0 operon) similar to genes coding for components of the main terminal branch of the general secretory pathway (e.g., the Klebsiella oxytoca pulC-0 pullulanase secretion operon) and to related genes required for type IV pilus biogenesis. For example, the last gene in the gsp operon, gspO (formerly hopD), encodes a protein which is similar to several type IV prepilin peptidases. Expression of gspO from lacZp promotes cleavage of two known prepilin peptidase substrates in E. coli K-12: Neisseria gonorrhoeae type IV prepilin and K. oxytoca prePulG protein. gspO also complements a mutation in the corresponding gene (pulO) of the pullulanase secretion operon when it is expressed from lacZp. Another gene in the gsp operon, gspG (formerly hopG), encodes a protein similar to prePulG, a component of the pullulanase secretion pathway. Expression of gspG from lacZp leads to production of a protein which (i) is recognized by PulG-specific antiserum (and by antiserum against the Pseudomonas aeruginosa PulG homolog XcpG [formerly XcpT]), (ii) is processed in cells expressing gspO, and (iii) restores secretion in cells carrying a pulG mutation. The chromosomal copies of gspG and gspO are apparently not expressed, probably because of very weak transcription from the upstream region, as measured by using a chromosomal gspC-lacZ operon fusion. Thus, the gsp operon of E. coli K-12 includes at least two functional genes which, together with the rest of the operon, are probably not expressed under laboratory conditions.

Bacterial Outer Membrane Proteins↗
PubMed2003

Common and distinguishing regulatory and expression characteristics of the highly related KorB proteins of streptomycete plasmids pIJ101 and pSB24.2.

The conjugative plasmid pIJ101 of the spore-forming bacterium Streptomyces lividans contains a regulatory gene, korB, whose product is required to repress potentially lethal expression of the pIJ101 kilB gene. The KorB protein also autoregulates korB gene expression and may be involved in control of pIJ101 copy number. KorB (pIJ101) is expressed as a 10-kDa protein in S. lividans that is immediately processed to a mature 6-kDa repressor molecule. The conjugative Streptomyces cyanogenus plasmid pSB24.1 is deleted upon entry into S. lividans to form pSB24.2, a nonconjugative derivative that contains a korB gene nearly identical to that of pIJ101. Previous evidence that korB of pSB24.2 is capable of overriding pIJ101 kilB-associated lethality supported the notion that pIJ101 and pSB24.2 encode highly related, perhaps even identical conjugation systems. Here we show that KorB (pIJ101) and KorB (pSB24.2) repress transcription from the pIJ101 kilB promoter equally well, although differences exist with respect to their interactions with kilB promoter sequences. Despite high sequence and functional similarities, KorB (pSB24.2) was found to exist as multiple stable forms ranging in size from 10 to 6 kDa both in S. lividans and S. cyanogenus. Immediate processing of KorB (pIJ101) exclusively to the 6-kDa repressor form meanwhile was conserved between the two species. A feature common to both proteins was a marked increase in expression or accumulation upon sporulation, an occurrence that may indicate a particular need for increased quantities of this regulatory protein upon spore germination and resumption of active growth of plasmid-containing cells.

Bacterial Proteins↗
PubMed1991

Pseudorabies virus mutants lacking the essential glycoprotein gII can be complemented by glycoprotein gI of bovine herpesvirus 1.

The genome of pseudorabies virus (PrV) encodes at least seven glycoproteins. The glycoprotein complex gII consists of three related polypeptides, two of them derived by proteolytic cleavage from a common precursor and linked via disulfide bonds. It is homologous to herpes simplex virus (HSV) gB and is therefore thought to be essential for PrV replication, as is gB for HSV replication. To isolate PrV mutants deficient in gII expression, we established cell lines that stably carry the PrV gII gene. Line N7, of Vero cell origin, contains the gII gene under its own promoter and expresses gII after transactivation by herpesviral functions after infection. MDBK-derived line MT3 contains the gII gene under control of the mouse metallothionein promoter. However, it has essentially lost inducibility and constitutively produces high amounts of correctly processed glycoprotein gII. We used a beta-galactosidase expression cassette inserted into a partially deleted cloned copy of the gII gene for cotransfection with PrV DNA. gII- PrV mutants were isolated from viral progeny by taking advantage of their blue-plaque phenotype when incubated under an agarose overlay containing a chromogenic substrate. Analysis of these mutants proved that gII is indeed essential for PrV replication, since the gII- mutants grew normally on gII-complementing cells but were unable to produce plaques on noncomplementing cells. Surprisingly the PrV gII- mutants were also able to grow on a cell line constitutively expressing the gB-homologous glycoprotein gI from bovine herpesvirus 1 (BHV-1) to the same extent as on cells expressing PrV gII. gII- PrV propagated on cells expressing BHV-1 gI became susceptible to neutralization by anti-BHV-1 gI monoclonal antibodies. We also found that BHV-1 gI is present in the envelope of purified gII- pseudorabies virions grown on cells expressing BHV-1 gI, as judged by radioimmunoprecipitation and immunoelectron microscopy. These results prove that BHV-1 gI is integrated into the PrV envelope and can functionally replace glycoprotein gII of PrV.

Animals↗
PubMed1997

Effects of mutations within and adjacent to the terminal repeats of hepatitis B virus pregenomic RNA on viral DNA synthesis.

The viral polymerase and several cis-acting sequences are essential for hepadnaviral DNA replication, but additional host factors are likely to be involved in this process. We previously identified two sequences, UBS and DBS (upstream and downstream binding sites), present in multiple copies in and adjacent to the pregenomic RNA (pgRNA) terminal redundancy, that were specifically recognized by a 65-kDa host factor, p65. The possible roles of these two sequences in hepatitis B virus (HBV) replication were investigated in the context of the intact viral genome. UBS is contained within the terminal redundancy of pgRNA, and the 5' copy of this sequence is essential for viral replication. Mutations within the central core of UBS ablate p65 binding and selectively block synthesis of plus-strand DNA, without affecting RNA packaging or minus-strand synthesis. The DBS sequence, which is located downstream of the pgRNA polyadenylation site, overlaps the core (C) protein coding region. All mutations introduced into this site severely affected viral replication. However, these effects were shown to result from dominant negative effects of mutant core polypeptides rather than from cis-acting effects on RNA recognition. Thus, the 5' UBS but not DBS sites play important cis-acting roles in HBV DNA replication; however, the involvement of p65 in these roles remains a matter for investigation.

Cells, Cultured↗