Biomedical subjects

H Fan

Publications and source records attributed to H Fan.

At least 145 records · Page 8Linked to original sources

PubMed1995

Disulfide bonds, N-glycosylation and transmembrane topology of skeletal muscle triadin.

Native triadin is a disulfide linked homopolymer of variable subunit number. Two monoclonal antibodies (mAbs), AE8.91 and GE4.90, recognize cytoplasmic regions of triadin between amino acids 110 and 163 and at the C-terminal 34 amino acids, respectively. Triadin in intact triads is largely unaffected by trypsin, while triads whose membrane has been disrupted by hypotonicity or by treatment with the detergent Triton X-100 yield both soluble and membrane bound fragments. Soluble fragments monitored by mAb GE4.90 appear to be formed sequentially during the course of proteolysis at 28, 16, 10 and 7 kDa in the presence of mercaptoethanol. Higher molecular weight bands are observed under nonreducing conditions. A two-dimensional electrophoresis immunoblot (first nonreducing; second reducing) of the soluble fragments developed with mAb GE4.90 shows the presence of several bands which can be interpreted as containing a dimer formed by a combination of any two of the fragments of 16, 10, or 7 kDa present in the digest. MAb AE8.91 does not detect these fragments. This observation indicates that one of the intermolecular disulfide bonds is formed between the identical domains of two triadin molecules at cysteine 671. Immunoblots performed with and without mercaptoethanol of the insoluble fragments using mAb AE8.91 indicate the presence of a dimer formed between identical domains of two triadin intermolecular disulfide linkage at cysteine 270. The glycosidase endo F/N-glycosidase F changed the mobility of intact triadin in TC/triads and its proteolytic fragments detected by mAb GE4.90.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMed1995

A model for mixed virus disease: co-infection with Moloney murine leukemia virus potentiates runting induced by polyomavirus (A2 strain) in Balb/c and NIH Swiss mice.

Polyomavirus was originally isolated by Ludwick Gross from a mixture that also contained a murine retrovirus. A possible pathogenic interaction between polyomavirus and an endogenous mouse retrovirus locus (mtv-7) in polyomavirus-induced cancer has also been reported. To study potential interactive effects of polyomavirus (Py) and Moloney murine leukemia retrovirus (M-MuLV), newborn Balb/c and NIH Swiss mice were infected with high titer wild-type Py (A2 strain) and M-MuLV. Dramatically stunted growth (runting) occurred in 100% of the doubly inoculated mice, while much lower frequency of runting occurred in animals infected with Py alone and not at all with M-MuLV-infected mice. In situ hybridization for Py DNA showed ongoing Py replication and inflammation in kidneys (atypical of most mice singly infected by Py) of runted doubly inoculated mice. In addition, high Py viral replication continued well past the usual acute stage termination. M-MuLV replication was also initially inhibited in bone marrow by simultaneous Py infection. No M-MuLV replication was seen in singly or doubly infected mouse kidneys. Runting was very rapid, observable within 2 days after co-infection, arguing against an adaptive or antigen-specific immunological mechanism. One possibility was that a cytokine-driven acute response mechanism was involved. Supporting this view, RNAse protection assays for various cytokine RNAs showed that several were specifically elevated in kidneys of doubly infected mice. Three patterns were observed: (1) IL-6 was elevated in doubly infected mice early after infection (7 days), but it declined at later times (19 days); (2) IFN-gamma, IL-1 beta, and IL-10 were elevated at both early and late times; and (3) TNF-alpha, IL-12p40, and possibly TNF-beta were elevated only at late times. While the cytokines in the third category might be indicative of infiltrating inflammatory cells, it seems possible that cytokines in the first or second categories might be involved in establishing runting and ongoing polyoma DNA replication in the doubly infected mice.

Animals↗

PubMed1995

Biological characterization and molecular cloning of murine C-type retroviruses derived from the TSZ complex from mainland China.

Characterization of the SRS murine retrovirus complex, derived from the TSZ system of murine leukemia developed in China, was carried out. The initial stock contained XC+, NB-tropic virus (and possibly other viruses), and induced several neoplastic diseases in neonatally inoculated NIH Swiss mice: erythroid leukemia, myeloid leukemia (acute myeloblastic leukemia), and lymphoblastic lymphoma (both B- and T-lymphoid). In addition, approximately 30% of inoculated animals developed central nervous system disease--hindlimb paralysis or semilateral paralysis. Rescue of virus from the spleen of an animal with combined erythroid/myeloid leukemia, followed by endpoint dilution gave two stocks: 19-6 (XC+, NB-tropic) and 19-7 (XC-, NB-tropic). Both stocks induced erythroid and myeloid leukemia, and 19-6 induced CNS symptoms as well. Southern blot analysis indicated that the predominant viruses from the 19-6 and the 19-7 cultures were related, but different in the env region. An infectious virus molecular clone of provirus from 19-6 cells was obtained. The resulting cloned virus [SRS 19-6 murine leukemia virus (MuLV)] induced four kinds of leukemia: erythroid, myeloid, B-lymphoma, and T-lymphoma; in many cases, more than one tumor type was identified in the same animal. Such a broad spectrum of leukemias induced by a cloned MuLV is unusual. Flaccid hindlimb paralysis induced by SRS 19-6 MuLV could be attributed to meningeal B-lymphoma. Immunofluorescent staining with a panel of env-specific monoclonal antibodies confirmed that the 19-6 and 19-7 viral stocks contained different viruses, which differed from previously characterized MuLVs. The viruses of the SRS complex may provide interesting reagents for investigations of MuLV-induced disease.

Animals↗

PubMed1995

Regulated expression of the obese gene product (leptin) in white adipose tissue and 3T3-L1 adipocytes.

A mutation within the obese gene was recently identified as the genetic basis for obesity in the ob/ob mouse. The obese gene product, leptin, is a 16-kDa protein expressed predominantly in adipose tissue. Consistent with leptin's postulated role as an extracellular signaling protein, human embryonic kidney 293 cells transfected with the obese gene secreted leptin with minimal intracellular accumulation. Upon differentiation of 3T3-L1 preadipocytes into adipocytes, the leptin mRNA was expressed concomitant with mRNAs encoding adipocyte marker proteins. A factor(s) present in calf serum markedly activated expression of leptin by fully differentiated 3T3-L1 adipocytes. A 16-hr fast decreased (by approximately 85%) the leptin mRNA level of adipose tissue of lean (ob/+ or +/+) mice but had no effect on the approximately 4-fold higher level in obese (ob/ob) littermates. Since the mutation at the ob locus fails to produce the functional protein, yet its cognate mRNA is overproduced, it appears that leptin is necessary for its own downregulation. Leptin mRNA was also suppressed in adipose tissue of rats during a 16-hr fast and was rapidly induced during a 4-hr refeeding period. Insulin deficiency provoked by streptozotocin also markedly down-regulated leptin mRNA and this suppression was rapidly reversed by insulin. These results suggest that insulin may regulate the expression of leptin.

3T3 Cells↗

PubMed1995

cDNA cloning and tissue-specific regulation of expression of rat calcium-binding protein 65/67. Identification as a homologue of annexin VI.

We isolated a cDNA encoding the rat membrane-associated 65/67-kDa calcium-binding protein, CBP 65/67, from a lambda ZAP II cDNA-expression library of rat liver by immunoscreening using monospecific polyclonal anti-(CBP 65/67) antibodies and monoclonal anti-(CBP 65/67) IgG. The product of this cDNA expressed in Escherichia coli was confirmed as CBP 65/67 both by immunostaining and by comparison of the molecular mass with the CBP 65/67 isolated from rat liver by SDS/PAGE. The cDNA sequence and the deduced amino acid sequence of CBP 65/67 both show a high degree of identity to human p68 and human calelectrin, which belong to a family of calcium-dependent, membrane-associated, phospholipid-binding proteins, called annexins. This means that CBP 65/67 is a homolog of the two human proteins just mentioned above. We are not aware that a rat annexin VI has previously been isolated and sequenced. The mRNA expression of CBP 65/67 in different rat organs during development was investigated by Northern blot analysis. In adult tissues, high mRNA levels of CBP 65/67 were found in lung, heart, muscle, spleen and especially in thymus and pancreas, whereas in liver, kidney, intestine, stomach and brain only low levels of CBP 65/67 mRNA could be detected. The amount of mRNA during tissue development in kidney, stomach and muscle showed only slight changes. In contrast, a significant increase of CBP 65/67 expression was observed in liver, lung, heart and brain. In most of the organs investigated, the level of mRNA correlated closely with the level of protein expression, indicating that the expression of CBP 65/67 in most organs is controlled primarily at the transcriptional level.

Amino Acid Sequence↗

PubMed1995

A plant basal in vitro system supporting accurate transcription of both RNA polymerase II- and III-dependent genes: supplement of green leaf component(s) drives accurate transcription of a light-responsive rbcS gene.

An in vitro transcription initiation system has been developed from nuclei of rapidly growing, non-green tobacco (Nicotiana tabacum) cultured (BY-2) cells. Conditions for nuclear extraction and in vitro transcription reaction have been optimized with a tobacco beta-1,3-glucanase gene, a constitutively expressed gene in BY-2 cells. The in vitro system supports accurate transcription of RNA polymerase II-dependent promoters from not only plant genes (tobacco beta-1,3-glucanase gene, cauliflower mosaic virus 35S promoter) but also animal genes (adenovirus 2 major late promoter, simian virus 40 early major promoter). In addition, this system drives accurate transcription of an RNA polymerase III-dependent Arabidopsis thaliana U6 snRNA gene. As BY-2 cells do not differentiate in response to light or any other stimuli, they would provide a basal transcription system which lacks tissue-specific and light-responsive nuclear signals as well as chloroplast-derived signals. Consequently, the BY-2 cell-free system is unable to transcribe the tomato gene encoding the small subunit of ribulose-1,5-bisphosphate carboxylase/oxygenase (rbcS3C) whose expression is tissue-specific and light-inducible. However, the transcription of rbcS3C was obtained by supplementing the BY-2 system with a nuclear extract of light-grown tomato seedlings. The promoter regions necessary for rbcS transcription was mapped in vitro using a series of 5' deletion mutants. The 351 bp upstream sequence is essential and the further upstream region from -351 to -441 enhances its transcription. The in vitro basal system will be useful to identify specific signals from both the nucleus and chloroplast in green leaves and other organs/tissues.

Arabidopsis↗

PubMed1995

Stage-specific induction of terminal deoxynucleotidyl transferase in a T-lymphoid line upon coculture with a thymic stromal line.

We previously reported an in vitro T-cell differentiation system in which the L4 lymphoid clone was cocultured with the St3 stromal line derived from the same murine thymic tumor, 15#4T.L4 cells in L4-St3 cocultures sequentially express Thy-1 and CD4 in a manner typical of normal thymocytes. In contrast, L4 cells grown in medium alone retain their Thy-1-CD4- phenotype. We also isolated L4 subclones from the coculture with increasingly differentiated phenotypes with respect to Thy-1 and CD4. We now report induction of an additional thymocyte differentiation marker, terminal deoxynucleotidyl transferase (TdT) in 15#4T cells (and to a lesser extent subcloned L4 cells) upon coculture with St3 stroma. Coculture of 15#4T cells with St3 stroma resulted in expression of TdT as measured by ribonuclease protection for TdT RNA and Western immunoblotting for TdT protein. Cocultured L4 cells were induced for TdT expression to a lesser degree and for a shorter period of time. The magnitude of TdT RNA induction was maximal for cell lines with the least mature differentiation phenotype (15#4T and L4: Thy-1-CD4-) and decreased proportionally for subclones with increasingly mature phenotype, e.g., L4E cells (Thy-1+CD4+). TdT protein was undetectable by Western immunoblotting and immunofluorescent staining of the L4E subclone on or off stroma. Recombination-activating gene-1 (RAG-1), which is expressed in immature thymocytes during T-cell receptor rearrangement, but suppressed in mature thymocytes, was also examined using the ribonuclease protection assay.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

In vitro transcription of plant RNA polymerase I-dependent rRNA genes is species-specific.

An in vitro transcription system derived from tobacco (Nicotiana tabacum) cultured cell (BY-2) nuclei supports transcription of the RNA polymerase I-dependent tobacco rRNA gene. The transcription initiation site determined in vitro was found at residue A which corresponds to that lying within the consensus sequence surrounding plant pre-rRNA initiation sites. The tobacco rRNA gene is actively transcribed in the tobacco nuclear extract while the broad bean rRNA gene is inactive in the heterologous system, indicating that plant RNA polymerase I-dependent transcription is species-specific.

Base Sequence↗

PubMed1995

Bradyrhizobium liaoningense sp. nov., isolated from the root nodules of soybeans.

Seventeen strains of extra-slowly growing (ESG) soybean rhizobia isolated from root nodules of Glycine soja and Glycine max growing in five provinces (Liaoning, Heilongjiang, Shanxi, Hubei, and Anhui) in the People's Republic of China were compared with 48 reference strains belonging to the genera Bradyrhizobium, Rhizobium, and Agrobacterium by performing a numerical analysis of 191 phenotypic features. Our results showed that all of the ESG strains examined clustered closely in the genus Bradyrhizobium but were separated from Bradyrhizobium japonicum at the species level and that they could be differentiated from Rhizobium and Agrobacterium species at the genus level. On the basis of the results of our numerical taxonomy analysis, a genomic DNA G & C content analysis, DNA-DNA hybridization experiments, a partial 16S rRNA sequence analysis, a serological analysis, an N and C content analysis, and an N/C ratio analysis of members of the three groups of soybean rhizobia, we propose the name Bradyrhizobium liaoningense sp. nov. for the ESG strains; the type strain of this species is strain 2281.

Base Composition↗

PubMed1995

Leukaemogenesis by the delta Mo + SV Moloney murine leukaemia virus (M-MuLV) variant in E mu pim-1 transgenic mice: high frequency of recombination with a solo endogenous M-MuLV LTR in vivo.

We previously described an enhancer variant of Moloney murine leukaemia virus (M-MuLV), delta Mo + SV M-MuLV, in which the enhancers of MuLV have been deleted and replaced with the enhancers of the simian virus 40 (SV40). When this virus is injected into neonatal NIH Swiss mice, pre-B and B-lymphoblastic lymphomas develop with a latency of 17 months. Van Lohuizen et al. (1989) described a line of transgenic mice that carry an activated pim-1 proto-oncogene transgene (E mu pim-1). They also reported that E mu pim-1 transgenic mice show greatly accelerated lymphoma development when infected with wild-type M-MuLV at birth. In these experiments, neonatal E mu pim-1 transgenic mice were infected intraperitoneally with delta Mo + SV M-MuLV. Marked acceleration of T-lymphoid leukaemia was seen. However, 10 of the 11 tumours analysed were found to be negative for the SV40 enhancers, but they still contained M-MuLV DNA as measured by Southern blot analysis. The LTRs on viruses cloned from two such tumours (as well as on virus recovered by infection onto NIH 3T3 cells) were characterized by PCR amplification, molecular cloning and sequence analysis. The LTR's from the two tumours were identical to each other and were distinct from both the delta Mo + SV M-MuLV and wild-type M-MuLV LTRs. However, they were identical to a rearranged solo M-MuLV LTR present in the E mu pim-1 transgene. These results indicate that the recombination in vivo between delta Mo + SV M-MuLV and the E mu pim-1 transgene yielded a replication-competent and pathogenic virus at high efficiency. This is the first report of in vivo recombination between an exogenous MuLV and a solo endogenous LTR.

Animals↗

PubMed1995

Identification of the Chlamydia trachomatis RecA-encoding gene.

DNA sequencing of the major outer membrane protein (MOMP) gene (omp1) from Chlamydia trachomatis shows that some strains have a mosaic structure suggestive of homologous recombination between two distinct omp1 genes. On the basis of this conjecture, we attempted to clone by complementation and sequence the chlamydial recA homolog from C. trachomatis serovar L2. Chlamydial genomic DNA was partially restricted with XbaI, and fragments of 2 to 4 kb were ligated into pUC19. The recombinant plasmid was electroporated into Escherichia coli HB101 (RecA-), and colonies were selected in the presence of methyl methanesulfonate (MMS). A 2.1-kb fragment of C. trachomatis DNA in pUC19 conferred relative MMS resistance to E. coli HB101. When this recombinant plasmid (pX203) was electroporated into E. coli JC14604 (RecA- lacZ), lac+ recombinants were isolated. Rabbit polyclonal antibodies produced to purified E. coli RecA were immunoreactive in an immunoblot assay with a 35-kDa antigen in RecA- strains of E. coli transformed with pX203. The 2.1-kb insert was cycle sequenced by the dideoxy chain termination method. An open reading frame of 1,056 bp encoding 352 amino acids that had 44% sequence identity with E. coli RecA was identified. The finding of a recA homolog in C. trachomatis suggests that homologous recombination may occur in this organism. The cloned C. trachomatis RecA-encoding gene will be useful for the construction of a recA mutant once a gene transfer system is developed for chlamydiae.

Amino Acid Sequence↗

PubMed1995

Recombinant mink cell focus-inducing virus and long terminal repeat alterations accompany the increased leukemogenicity of the Mo+PyF101 variant of Moloney murine leukemia virus after intraperitoneal inoculation.

We recently showed that different routes of inoculation affect the leukemogenicity of the Mo+PyF101 variant of Moloney murine leukemia virus (M-MuLV). Intraperitoneal (i.p.) inoculation of neonatal mice with Mo+PyF101 M-MuLV greatly enhanced its leukemogenicity compared with subcutaneous (s.c.) inoculation. We previously also suggested that the leukemogenicity defect of Mo+PyF101 M-MuLV when inoculated s.c. may result from the inability of this virus to form env gene recombinant (mink cell focus-inducing [MCF]) virus. In this study, virus present in end-stage tumors and in preleukemic animals inoculated i.p. by Mo+PyF101 M-MuLV was characterized. In contrast to s.c. inoculation, all tumors from i.p.-inoculated mice contained high levels of recombinant MCF virus. Furthermore, Southern blot analyses demonstrated that the majority of the tumors contained altered Mo+PyF101 M-MuLV long terminal repeats. The U3 regions from several tumors with altered long terminal repeats were cloned by PCR amplification. Sequence analyses indicated that the M-MuLV 75-bp tandem repeat in the enhancer region was triplicated. This amplification was also previously observed in mice infected s.c. with a pseudotypic mixture of Mo+PyF101 M-MuLV and Mo+PyF101 MCF virus. The enhancer triplication was an early event, and it occurred within 2 weeks postinfection. Recombinant MCF viruses were not detected by Southern blot analyses until 4 weeks postinfection. Thus, the M-MuLV enhancer triplication event was initially important for efficient propagation of ecotropic Mo+PyF101 M-MuLV. The increased leukemogenicity following i.p. inoculation could be explained if the triplication enhances Mo+PyF101 M-MuLV replication in the bone marrow and bone marrow infection is required for recombinant MCF virus formation.

3T3 Cells↗

PubMed1995

Proviral activation of the c-myb proto-oncogene is detectable in preleukemic mice infected neonatally with Moloney murine leukemia virus but not in resulting end stage T lymphomas.

Moloney murine leukemia virus induces myeloid leukemia when inoculated intravenously into pristane-primed adult BALB/c mice. One hundred percent of these tumors show insertional activation of the c-myb proto-oncogene, and reverse transcriptase PCR assays have shown that the c-myb activation could be detected soon after infection. We tested BALB/c and NIH Swiss mice that had been inoculated as newborns with Moloney murine leukemia virus, under which conditions they develop T lymphomas exclusively. Reverse transcriptase-PCR assays indicated that c-myb activations were detectable soon after neonatal infection. However, none of the resulting T lymphomas contained c-myb activations. The implications of these results to the timing of proto-oncogene activations in leukemogenesis and the specificity of proto-oncogene activations for different diseases are discussed.

Animals↗

PubMed1995

The effects of passive anti-viral immunotherapy in AKR mice: II. Susceptibility to B cell lymphomagenesis.

Prevention of high frequency spontaneous T cell lymphoma development in AKR mice by mAb 18-5 treatment was shown to involve inhibition of the recombinant Class I MCF virus formation and elimination of the early occurring potential lymphoma cells (PLCs). A low B cell lymphoma incidence (16% at a mean latency of 540 days) and a low level of PLCs (yielding 12% B cell lymphoma development following lymphoid cell transfer) was observed in mAb 18-5 treated mice (in contrast to a high PLC level in thymectomized AKR mice that could be experimentally triggered to progress to overt CD5+ B cell lymphomas). Administration of anti CD8 mAb or IL-4 to 12-month-old mAb 18-5 pre-treated mice only slightly increased B cell lymphoma incidence (up to 30-40%). Exposure to split-dose irradiation resulted in 26% B cell lymphomas at a 250 day mean latency. The phenotypes of the B lymphomas developing in mAb 18-5 treated mice were: B220+ (14.8+, 6B2+), 6C3+, Mac2+, CD5-. Most lymphomas expressed l-a and surface IgM, pointing to their mature B cell characteristics. Moreover, in some of the lymphomas, high levels of IgM production and secretion were determined. A comparison of the morphological characteristics (based on light and ultrastructure microscopy) of CD5+ and CD5- B cell lymphomas developing in AKR mice indicated marked differences. Analysis of the IgH locus of representative CD5- B lymphomas showed an identical pattern of IgH rearrangement in some tumors (similar to previous findings among CD5+ lymphomas). The virological analysis of the CD5- B cell lymphomas (similar to those observed in the CD5+ B cell lymphomas of AKR origin) showed that their development did not require formation of the pathogenic MCF recombinant viruses. The differences observed between the CD5+ and CD5- B cell lymphomas developing in AKR mice (following prevention of spontaneous T cell lymphomagenesis) may be due to their origin of different B cell precursors or from B cells at different levels of differentiation.

Animals↗

PubMed1995

Evaluation of serum troponin T measurement in acute myocardial infarction.

The release kinetics of the cardiac specific troponin T (cTnT), measured by an immunosorbent assay, in 32 patients with acute myocardial infarction (AMI) was evaluated. In 8 AMI patients (25%), the release kinetics of serum cTnT showed biphasic serum concentration curves with a large peak at 10 to 18 hours after onset and the serum cTnT concentrations were up to 30 to 120 times of the normal upper limit-detected (0.2 microgram/ml), and another samll cTnT peak at 70 to 100 hours after onset of pain. The serum cTnT measurements in the remaining 24 AMI patients (75%) gave only one large peak which was around 32 to 108 hours after onset of pain. cTnT appeared in serum as early as 3 to 4 hours and remained elevated until 240 hours after the infarctions. The results indicated that (1) cTnT was a sensitive and specific marker of AMI; (2) the biphasic curve of cTnT releae in general, the ratio of cTnT at around 14 to 32 (14/32) > 1 in particular, may be a useful marker suggesting early reperfusion; (3) the continuous elevation of serum cTnT in AMI course might be a prognostic indicator for unfavorable outcomes.

Aged↗

PubMed1995

The effects of passive antiviral immunotherapy in AKR mice: I. The susceptibility of AKR mice to spontaneous and induced T cell lymphomagenesis.

The AKR inbred mouse strain displays a high incidence of spontaneous T cell lymphomas that arise predominantly in the thymus of 6 to 12-month-old mice. Heterogenous nonacute transforming retroviruses are associated with the etiology of the disease: the endogenous ecotropic viruses (inherited in AKR mice at two non-linked chromosomal loci, Akv-1 and Akv-2), the xenotropic virus and recombinant viruses. Prevention of spontaneous T cell lymphomagenesis in AKR mice by passive anti-viral immunotherapy was accomplished by suppressing endogenous ecotropic virus release. Treatment with monoclonal antibody Hy-72 reacting only with Akv1 type ecotropic viruses, or with mAb 18-5 with specificity for both ecotropic and MCF recombinant virus envelope glycoprotein (administered from birth for 10 days) inhibited similarly T cell lymphoma development. A reduced thymus cellularity observed in these mAb treated mice coincided with reduced level of earliest intrathymic low CD4 precursor population in their thymus. The role of endogenous viruses (MuLV) and presence of potential lymphoma cells (PLCs) (identified among bone marrow cells of untreated AKR mice) in enhanced T cell lymphomagenesis in AKR mice, triggered by different leukemogenic agents, was evaluated. Intrathymic injection of the radiation leukemia virus variant A-RadLV or administration of methylnitrosourea resulted in a high lymphoma incidence within a short latent period of 80-100 days irrespective of the presence or absence of MuLV or PLCs in these treated mice. Thus, a direct action of these agents on thymocytes seems to occur. The high susceptibility of untreated AKR mice to radiation induced T cell lymphomagenesis was not affected by pretreatment with mAb Hy-72; in contrast to markedly reduced sensitivity following pretreatment with mAb 18-5 (15 vs 100%). The mAb 18-5 induced resistance to radiation lymphomagenesis seems to be related to defects in the bone marrow stem cell pool as well as in the thymus microenvironment of mAb 18-5 treated mice. Thus, different developmental pathways are involved in enhanced T cell lymphomagenesis in AKR mice.

Animals↗

PubMed1994

Identification of annexin 33 kDa in cultured cells as a binding protein of influenza viruses.

The binding of three influenza A and one influenza B virus strains to proteins of three continuously cultured cell lines was studied using protein overlay and immunostaining methods. The results obtained indicated the presence of both sialic acid-dependent and -independent binding of the virus strains; virus binding to proteins in the molecular mass range from about 40 to 103 kDa was dependent on sialic acid, whereas binding to the 33 kDa protein was independent of sialic acid. The 33 kDa binding protein was identified as annexin, a widely distributed non-glycosylated calcium-dependent phospholipid-binding protein.

Animals↗

PubMed1994

Structural diversity of triadin in skeletal muscle and evidence of its existence in heart.

Triadin has been characterized as an abundant protein co-localized with the calcium release channel on the terminal cisternae of the sarcoplasmic reticulum of the skeletal muscle. Its localization to terminal cisternae of the sarcoplasmic reticulum and functional studies suggest that it has an important role in excitation-contraction coupling. In this study we identify three triadin isoforms in rabbit skeletal muscle and by Northern blot analysis demonstrate that triadin also exists in the heart.

Amino Acid Sequence↗