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At least 199 records · Page 11Linked to original sources
PubMed2003

Involvement of the histone deacetylase SIRT1 in chicken ovalbumin upstream promoter transcription factor (COUP-TF)-interacting protein 2-mediated transcriptional repression.

Chicken ovalbumin upstream promoter transcription factor (COUP-TF)-interacting proteins 1 and 2 (CTIP1 and CTIP2) enhance transcriptional repression mediated by COUP-TF II and have been implicated in hematopoietic cell development and malignancies. CTIP1 and CTIP2 are also sequence-specific DNA-binding proteins that repress transcription through direct, COUP-TF-in-dependent binding to a GC-rich response element. CTIP1- and CTIP2-mediated transcriptional repression is insensitive to trichostatin A, an inhibitor of known class I and II histone deacetylases. However, chromatin immunoprecipitation assays revealed that expression of CTIP2 in mammalian cells resulted in deacetylation of histones H3 and/or H4 that were associated with the promoter region of a reporter gene. CTIP2-mediated transcriptional repression, as well as deacetylation of promoter-associated histones H3/H4 in CTIP2-transfected cells, was reversed by nicotinamide, an inhibitor of class III histone deacetylases such as the mammalian homologs of yeast Silent Information Regulator 2 (Sir2). The human homolog of yeast Sir2, SIRT1, was found to interact directly with CTIP2 and was recruited to the promoter template in a CTIP2-dependent manner. Moreover, SIRT1 enhanced the deacetylation of template-associated histones H3/H4 in CTIP2-transfected cells, and stimulated CTIP2-dependent transcriptional repression. Finally, endogenous SIRT1 and CTIP2 co-purified from Jurkat cell nuclear extracts in the context of a large (1-2 mDa) complex. These findings implicate SIRT1 as a histone H3/H4 deacetylase in mammalian cells and in transcriptional repression mediated by CTIP2.

COUP Transcription Factors↗
PubMed2004

HIV-1 Nef promotes survival of TF-1 macrophages by inducing Bcl-XL expression in an extracellular signal-regulated kinase-dependent manner.

The Nef protein of human immunodeficiency virus-1 (HIV-1) is essential for the progression from human and simian immunodeficiency virus infection to full-blown AIDS. Recent studies indicate that Nef generates anti-apoptotic signals in HIV-infected T cells, suppressing cell death early in infection to allow productive viral replication. Previous work from our laboratory has shown that Nef also promotes proliferation of myeloid cells through a signal transducer and activator of transcription 3-dependent pathway. Here we demonstrate that Nef suppresses cell death induced by cytokine deprivation in the human macrophage precursor cell line, TF-1. Nef selectively induced up-regulation of Bcl-XL, an anti-apoptotic gene that is also regulated by granulocyte/macrophage-colony stimulating factor in this cell line. Activation of the extracellular signal-regulated kinase (Erk) mitogen-activated protein kinase pathway also correlated with the survival of TF-1/Nef cells. Using the selective mitogen-activated protein kinase kinase inhibitor PD98059, we found that Nef-induced Erk signaling is essential for Bcl-XL up-regulation and cell survival. In contrast, expression of Bcl-XL and TF-1 survival was not affected by dominant-negative signal transducer and activator of transcription 3. These data suggest that Nef produces survival signals in myeloid cells through Erk-mediated Bcl-XL induction, a pathway distinct from Nef survival pathways recently reported in T lymphocytes.

Apoptosis↗
PubMed1990

The binding site for the liver-specific transcription factor Tf-LF1 and the TATA box of the human transferrin gene promoter are the only elements necessary to direct liver-specific transcription in vitro.

We have studied the liver-specific transcriptional activity of the human transferrin gene promoter. Results of competition experiments, site-directed mutagenesis, and 5' deletion analysis have demonstrated that a TATA box and a binding site for the liver-specific protein Tf-LF1 are the only elements needed to direct hepatic-specific transcription in vitro. Thus, Tf-LF1 behaves as other previously described proteins, HNF-1, DBP and LF-A1, in that it is sufficient to confer liver-specific transcriptional activity to a promoter in vitro. This results contrast with observations made in transient expression experiments, in which Tf-LF1 binding alone cannot direct hepatic-specific expression, and the binding of at least one more protein, similar to C/EBP, is needed. Thus, as described for other hepatic genes, the number of elements necessary to confer tissue specificity is different in vivo and in vitro.

Base Sequence↗
PubMed1987

Phage tf-1: a filamentous bacteriophage specific for bacteria harbouring the IncT plasmid pIN25.

Phage tf-1 is a filamentous phage which is about 800 nm in length, 10 nm in width and has slightly tapered ends. The phage was isolated from sewage and formed plaques or propagated only on Escherichia coli, Salmonella typhimurium and Klebsiella oxytoca strains harbouring the IncT plasmid pIN25 at 30 degrees C. It adsorbed in large numbers to pIN25-encoded long thick flexible conjugative pili formed at 30 degrees C and also to the short form of these pili synthesized at 37 degrees C. The reason for the failure to form plaques at 37 degrees C is not known. The adsorption site is a short length of the pilus shaft extending 100-200 nm back from the distal tip. Efficient phage tf-1 adsorption to the same site was found for pili determined by other IncT plasmids in spite of the fact that phage tf-1 did not plate or propagate on strains harbouring them. However, areas of specific partial clearing on lawns of these plasmid-containing bacteria were produced by phage in high concentrations. Lack of plaque-formation could be due to inefficient intracellular assembly coupled to avid adsorption of any liberated phage to pili. The phage differs from all but one other filamentous phage by being sensitive to diethyl ether.

Adsorption↗
PubMed1976

A transferrin variant Tf I in crosses of the wild and domestic pigs.

In crosses of the wild pig (Sus scrofa attila Thomas) with the domestic pig a transferrin variant, Tf I, was detected, electrophoretic mobility of which was slightly faster than the mobility of the variant Tf A. From the results of starch gel electrophoresis, isolation, neuraminidase treatment, autoradiography, and genetic analysis of several families, it can be concluded that the Tf I variant is genetically controlled by the allele Tf1. Thus the number of alleles in the transferrin system of the pig has increased to six (Tf1, TfA, TfB, TfC, TfD and TfE).

Animals↗
PubMedDate not supplied

A computational analysis of FXa generation by TF:FVIIa on the surface of rat vascular smooth muscle cells.

A computational model was developed to investigate the contribution of classical mass transport and flow parameters to factor X (FX) activation by the tissue factor-factor VIIa complex (TF:VIIa) on one wall of a parallel-plate flow chamber. The computational results were compared to previously obtained experimental data for the generation of factor Xa (FXa) by TF:VIIa on the surface of cultured rat vascular smooth muscle cells. In this study, the complete steady-state convection-diffusion equation was solved using the commercial software package, FLUENT (Fluent Inc., Lebanon, New Hampshire). A user-defined subroutine interfaced with FLUENT implemented the surface reaction which was modeled using classical Michaelis-Menten reaction kinetics. The numerical solutions were obtained for 12 cases which used combinations of three wall shear rates and four reaction rates. The numerically obtained fluxes for a given reaction rate displayed a wall shear rate dependence which ranged from classical kinetic reaction control (no dependence) to pure diffusional control (maximum dependence). The experimental data, however, were not represented by numerical data generated using a single reaction rate. The three numerically obtained fluxes which corresponded most closely to the experimental fluxes were determined using three different Vmax values. This finding supports the hypothesis that there may be a direct effect of flow on the TF:VIIa complex or the cell membrane.

Algorithms↗
PubMed1987

The sequence of chromosome 3 loci AHSG:TF:CHE1.

A large Hutterite kindred was examined for possible linkage between the chromosome 3 markers; cholinesterase (CHE1), transferrin (TF), and alpha-2HS glycoprotein (AHSG). Linkage between TF and AHSG was suggested in males (z = 1.515, theta = 0.08) and between CHE1 and TF(z = 0.661, theta = 0.21). However, linkage between CHE1 and AHSG in males was not established. Based on lods and a nuclear family informative for all three loci a possible chromosomal alignment for the loci is presented.

Cholinesterases↗
PubMed2000

Orphan receptors COUP-TF and DAX-1 as targets in disordered CYP17 expression in adrenocortical tumors.

CYP17 gene transcription is activated by SF-1 binding to a cyclic AMP-responsive sequence within the promoter region of the gene, and its transcription is inhibited by COUP-TF binding to the sequence. Another orphan receptor, DAX-1, is shown to act as a suppressor of SF-1-mediated transcription. We examined the expression level of these orphan receptors in adrenocortical tumors and compared the results with CYP17 expression. CYP17 was highly expressed in cortisol-producing adenomas, whereas COUP-TF and DAX-1 expression levels were very low. In deoxycorticosterone-producing adenomas, on the other hand, CYP17 expression was extremely low, whereas DAX-1 was highly expressed and SF-1 expression was slightly decreased. In conclusion, the reciprocal expression of CYP17 and the transcriptional repressors COUP-TF and DAX-1 indicates that these orphan receptors have a pathophysiologic role in the excessive hormone production in cortisol- and deoxycorticosterone-producing adrenocortical tumors.

Adrenal Cortex Neoplasms↗
PubMed2000

NGF-Tf Conjugate Prevents Degeneration of Substantia Nigra Neurons in a Mouse Model of Parkinson's Disease.

Nerve growth factor(NGF) was purified from Naja naja atra snake venom and conjugated to transferrin(Tf). This conjugate was intravenously injected into a mouse model of Parkinson's disease (PD). Both immunohistochemical staining and pathological detection showed that the NGF-Tf conjugate could prevent the loss of tyrosine hydroxylase-immunoreactive neurons located in substantia nigra and the cell counts of NGF group were 2 330.0+/-260.3, and those of the MPTP group and the control group were 797.0+/-121.4 and 2 381.0+/-158.0, respectively. In addition, electron microscopic examination revealed significant protection against demyelination and vacuolation in subtantia nigra neurons in contrast to the control group. The i.v. injected NGF-Tf conjugate also reversed the neurodegenerative changes such as karyopyknosis, chromatolysis and intracytoplasmic inclusion in diseased neurons.

Journal Article↗
PubMed2003

[Study on bonding strength of TF adhesive compounded with nanograde hydroxyapatite].

TF no-mix orthodontic adhesive was compounded in different weight proportion of nanograde hydroxyapatite as 10%, 20% and 30%, for use in this comparative study on composites. 80 orthodontic brackets were cemented and divided into 8 experimental groups, and TF adhesive was set as the control group. The tensile strength and shear strength were tested respectively. The results showed that the group of 10% nanograde hydroxyapatite obtained the greatest bonding strength (9.668 +/- 1.0649 MPa in tensile strength and 11.991 +/- 1.4135 MPa in shear strength), and there was significant difference between the 10% group and the other groups (P < 0.05, one-way ANAOV). It is concluded that the bonding strength can be enhanced when TF adhesive is compounded in suitable proportion of nanograde hydroxyapatitie.

Animals↗
PubMed1988

[Physical map of the DNA of bacteriophage tf of Pseudomonas putida].

A physical map has been constructed for P. putida bacteriophage tf DNA containing single-strand breaks (nicks). Localization of cleavage sites for EcoRI, HindIII, HpaI ClaI, BamHI, SalI, XbaI and XhoI restriction endonucleases was determined. Position of single-strand breaks was mapped by electrophoretic analysis of denatured tf DNA and electron microscopy of partially denatured DNA samples. The tf genome is characterized by the presence of two classes of nicks differing in the frequency of their presence in population of bacteriophage DNA molecules.

Bacteriophages↗
PubMed1995

Human interleukin-3 receptor modulates bcl-2 mRNA and protein levels through protein kinase C in TF-1 cells.

Upon withdrawal of interleukin-3 (IL-3) from human factor-dependent erythroleukemic cell line TF-1, bcl-2 mRNA and protein levels decrease within 8 to 24 hours. Accompanying this decrease is the onset of apoptosis as determined by flow cytometric analysis of DNA degradation. By 8 to 18 hours of deprivation approximately 70% to 80% of the cells have entered apoptosis. Downregulation of protein kinase (PK) by a 24-hour incubation in 100 nmol/L 12-O-tetradecanoyl-phorbol-13-acetate (TPA) in the presence of IL-3 dramatically reduced bcl-2 mRNA levels, and induced apoptosis in the presence of IL-3. We have also found that even in the presence of IL-3, two inhibitors of PKC, light-activated calphostin and H-7, substantially reduced the levels of bcl-2 mRNA between 8 and 24 hours as measured by a semi-quantitative reverse transcriptase/polymerase chain reaction assay method; however, the cyclic nucleotide-dependent PK inhibitor HA 1004, that is a structural analog of H-7 but a poor inhibitor of PKC, did not reduce bcl-2 levels in the presence of IL-3. This decrease in bcl-2 mRNA was accompanied by a decline in bcl-2 protein levels by 8 to 24 hours after addition of light-activated calphostin. In addition to interfering with the maintenance of bcl-2 mRNA levels, inhibition of PKC with H-7 inhibited the induction of bcl-2 mRNA in factor-deprived TF-1 cells restimulated with IL-3. The cyclic nucleotide-dependent PK inhibitor HA 1004 did not inhibit IL-3-induced bcl-2 mRNA. Studies with actinomycin D showed that transcription plays a major role in maintaining bcl-2 levels in TF-1 cells, and it is therefore likely that IL-3 plays a role in maintaining bcl-2 transcription through activation of PKC in these cells.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1997

Genetic study of African populations: polymorphisms of the plasma proteins TF, PL, F13B, and AHSG in populations of Namibia and Mozambique.

Genetic variations of four highly polymorphic serum proteins, TF, PI, F13B, and AHSG, were tested to distinguish one black African and one Khoisan population of southwest Africa. The results show that indeed the systems TF, PI, and AHSG are of high value for anthropological genetics: The allele frequencies for these systems enable clear identification of and distinction between black African and Khoisan populations. The F13B locus, on the other hand, reveals for both the black African and the Khoisan populations specific and unique African variants: a high frequency of F13B*2 and the lowest frequency of F13B*3 so far worldwide. The new data are compared with results for TF and PI in another black African population of Mozambique, which Rodewald et al. (1988) had studied previously. The dendrogram, based on genetic distance data D and average linkage cluster analysis, shows minimal distance between both black African populations of Namibia and Mozambique and marked distance between those and the Khoisan population of Namibia.

Alleles↗
PubMed1995

PML/RARalpha, a fusion protein in acute promyelocytic leukemia, prevents growth factor withdrawal-induced apoptosis in TF-1 cells.

A unique mRNA produced by the t(15;17) (q22-24;q11-21) translocation in the leukemic cells of acute promyelocytic leukemia patients encodes a chimeric protein, PML/RARalpha, which is formed by the fusion of the retinoic acid receptor alpha (RARalpha) and the promyelocytic locus gene (PML). This translocation is often the only visible karyotypic aberration present which is detected in almost 100% of acute promyelocytic leukemia patients. As an initial step to study the role of PML/RARalpha in leukemogenesis, we attempted to express the fusion protein in hematopoietic cells through retrovirus-mediated gene transfer of the retroviral vector, pGPRCHT, which contains the PML/RARalpha cDNA. Transduction of the PML/RARalpha cDNA fragment used in this vector, which extends from the position 31 bp to the position 2638 bp in a transcription unit driven by the Moloney murine sarcoma virus LTR, was found to abrogate the growth factor dependence of TF-1 cells. In addition, introduction of PML/RARalpha into TF-1 cells can protect these cells from the apoptosis usually induced in TF-1 cells by growth factor withdrawal, as measured by three assays for apoptosis: morphology, DNA ladder formation, and end labeling of nicked DNA with fluorescent-conjugated nucleotide precursors followed by a fluorescence-activated cell sorting assay. These data suggest that the PML/RARalpha fusion protein may inhibit programmed cell death in myeloid cells.

Apoptosis↗
PubMed1999

TFAR19, a novel apoptosis-related gene cloned from human leukemia cell line TF-1, could enhance apoptosis of some tumor cells induced by growth factor withdrawal.

Using the cDNA-representative differences analysis (cDNA-RDA) approach, we identified a novel gene, TFAR19 (TF-1 cell apoptosis related gene-19), from TF-1 cells undergoing apoptosis. The human TFAR19 encodes a protein which shares significant homology to the corresponding proteins of species ranging from yeast to mice. TFAR19 exhibits a ubiquitous expression pattern and its expression is upregulated in the tumor cells undergoing apoptosis. Overexpression of TFAR19 in tumor cells enhances apoptosis triggered by growth factor or serum deprivation. We propose that TFAR19 may play a general role in the apoptotic process.

Amino Acid Sequence↗
PubMed1981

Transferrin (Tf) subtyping on agarose: a new technique for isoelectric focusing.

Isoelectric focusing (IEF) of the serum protein transferrin (Tf) on polyacrylamide gels has been found to be a useful tool in population genetics and forensic medicine. Three autosomal codominant alleles can be subtyped from the TfC allele, TfC1, TfC2, and TfC3. In this report the authors describe the use of agarose as an alternative technique for Tf subtyping. The method is faster, easier to perform and eliminates the use of toxic chemicals used with polyacrylamide gels. Results of subtyping for the three alleles Tfc1, Tfc2, and Tfc3 are described for a population of U.S. whites (n = 392) and U.S. blacks (n = 194).

Acrylic Resins↗
PubMed1984

[Effect of the genetic markers Kell(K1), P1, Km(1), Tf(C<B<D), AK and 6-PGD on the outcome of paternity cases].

This statistical analysis of the results of 288 paternity cases is a contribution to the discussion of those blood group systems to be selected for the basis of paternity expertise in the Federal Republic of Germany. When typing 22 blood-group systems in 288 one-man cases, we found exclusions in 101 (35.07%) of them. In only 83 (44.39%) of the 187 cases with nonexclusions did the resulting EM value correspond to the verbal predicate: "paternity practically proved." The results of the systems of factors Kell(K1), Tf(C,B,D), AK and 6-PGD had the smallest rate of exclusion constellations and only inferior influence on the resulting EM values. Replacing them by isoelectric focusing of the systems PGM1, Tf, Gc, Pi and PLG (plasminogen) seems to be reasonable. The factors P1 and Km(1) proved more favorable for the results of paternity cases.

Blood Group Antigens↗