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F Marks

Publications and source records attributed to F Marks.

At least 127 records · Page 7Linked to original sources
PubMed1989

cDNA-cloning, sequencing and expression in glucocorticoid-stimulated quiescent Swiss 3T3 fibroblasts of mouse lipocortin I.

We isolated and sequenced mouse lipocortin I cDNA clones from a lambda gt10 cDNA library prepared from Swiss 3T3 mRNA. The homology with human lipocortin I at the amino acid level is 86%. When confluent layers of Swiss 3T3 cells were stimulated with 10% fetal calf serum, expression of lipocortin I was strongly stimulated. In parallel, DNA synthesis was induced with a peak at 24 hours after glucocorticoid treatment indicating induction of cell proliferation. In the absence of serum glucocorticoid treatment provoked neither induction of DNA synthesis nor expression of lipocortin I. We conclude that serum contains an unidentified factor, which acts synergistically with glucocorticoids on cell proliferation and lipocortin I expression.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1989

A phorbol ester and phospholipid-activated, calcium-unresponsive protein kinase in mouse epidermis: characterization and separation from protein kinase C.

The phosphorylation of an Mr 82,000 protein (p82) in the Triton X-100 extract of the particulate fraction of mouse epidermis is dependent on the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) or diacylglycerol and phospholipid and, contrary to protein kinase C (PKC)-catalyzed phosphorylation, cannot be activated by calcium plus phospholipid. The novel p82 kinase differs also from PKC in many other respects, such as substrate specificity, turnover rate, and sensitivity to inhibitors. The p82 kinase can be separated from PKC by chromatography on phenyl sepharose and does not react with a polyclonal PKC antiserum. Like PKC, the novel kinase phosphorylates its substrate on threonine and serine, but not on tyrosine. Similar to PKC, the epidermal p82-kinase system is down-modulated after TPA treatment of mouse skin, with a half-life of around 5 h. Down-modulation is also accomplished by the phorbol ester RPA, but not by the Ca2+ ionophore A23187, and it is inhibited by the immunosuppressive agent cyclosporin A. In addition to down-modulation, TPA treatment of the animals activates a phosphatase that dephosphorylates phosphorylated p82 in the extract of the particulate fraction.

Animals↗
PubMed1989

Congenital hereditary fructose intolerance and pregnancy.

Congenital hereditary fructose intolerance is associated with the inability to tolerate fructose and carbohydrates, which are converted into fructose. We describe management of a pregnancy complicated by this disease in the mother and its implications for the neonate.

Adult↗
PubMed1989

Cell cycle specificity and reversibility of the inhibitory effect of epidermal G1-chalone on DNA synthesis in partially synchronized RTE-2 keratinocytes in vitro.

The specific action of a pig skin fraction enriched in epidermal G1-chalone, a tissue-specific inhibitor of epidermal DNA synthesis, was investigated by means of flow cytofluorometry. The results indicate that G1-chalone inhibits progression of partially synchronized rat tongue epithelial cells (line RTE-2) through the cell cycle at a point 2 h prior to the beginning of the S-phase. Approximately 8 h after chalone addition, the cells can overcome the inhibition and begin to enter the S-phase. The duration of this delay is concentration-independent, but the fraction of cells affected is proportional to the chalone concentration. The progression of cells which already have entered S-phase is not affected. In contrast to the G1-chalone preparation, aphidicolin, a potent inhibitor of DNA polymerase alpha, clearly shows S-phase-specific inhibition. These results indicate that the epidermal G1-chalone inhibits epidermal cell proliferation in a fully reversible manner by a highly specific effect on cell cycle traverse.

Animals↗
PubMed1989

The immunosuppressant FK-506, like cyclosporins and didemnin B, inhibits calmodulin-dependent phosphorylation of the elongation factor 2 in vitro and biological effects of the phorbol ester TPA on mouse skin in vivo.

Similar to previous observations with cyclosporins and didemnin B, the novel immunosuppressant FK-506 inhibits the Ca2+/calmodulin-dependent phosphorylation of the eukaryotic elongation factor 2 of protein synthesis in vitro and biological effects of the phorbol ester TPA on mouse skin in vivo. These effects include the induction of the ear edema and the stimulation of alkaline phosphatase activity. FK-506 neither activates nor inhibits protein kinase C in vitro. FK-506 does not compete with cyclosporin A for the high-affinity binding sites in mouse epidermis cytosol.

Animals↗
PubMed1989

Eicosanoids and multistage carcinogenesis in NMRI mouse skin: role of prostaglandins E and F in conversion (first stage of tumor promotion) and promotion (second stage of tumor promotion).

When applied to NMRI mouse skin in vivo, phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and 12-O-retinoylphorbol-13-acetate (RPA) have been found to induce two early waves of prostaglandin E2 (PGE2) synthesis after 15 and 90 min and a delayed accumulation of prostaglandin F2 alpha (PGF2 alpha) after 2 h. With respect to PGF2 alpha formation different activities of both agents were observed, in that TPA but not RPA induced additional PGF2 alpha waves after 4 and 17 h. Functionally, PGE2 was previously shown to be an endogenous mediator of the TPA- or RPA-induced epidermal hyperproliferation and hyperplasia. A functional role of PGF2 alpha could be attributed to the post-initiation stages of tumor development in initiated mouse skin, i.e. the conversion stage (stage I of tumor promotion) elicited by two TPA applications and the promotion stage (stage II of promotion) brought about repetitive RPA treatments. PGF2 alpha, appearing as one distinct biosynthetic wave 3-4 h after TPA application seems to be critically involved in the conversion steps since (i) inhibition of its accumulation by indomethacin led to an inhibition of tumor formation, (ii) the inhibitory effect of indomethacin could be reversed by PGF2 alpha and (iii) RPA was not able to give rise to the accumulation of PGF2 alpha 4 h after application as obtained by TPA treatment. Moreover, RPA-induced promotion of DMBA- and TPA-treated mouse skin was inhibited by indomethacin. The inhibitory effect of indomethacin on papilloma formation was again reversed by PGF2 alpha treatment concomitant with RPA.

Animals↗
PubMed1989

Tumor induction in initiated mouse skin by phorbol esters and methyl methanesulfonate: correlation between chromosomal damage and conversion ('stage I of tumor promotion') in vivo.

Using the multistage (initiation-conversion-promotion) protocol we have studied the effects of methyl methanesulfonate (MMS), a well-known alkylating and clastogenic agent, on tumor development in NMRI mouse skin in vivo. When topically applied in a dose up to 400 mumol MMS did not exhibit any initiating efficacy while under identical conditions chromosomal damage (mainly breaks and gaps) was induced in epidermis. A dose of 100 mumol MMS was found to be almost as clastogenic as 10 nmol of the convertogenic tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), whereas the non-convertogenic promoter 12-O-retinoylphorbol-13-acetate (RPA, 10 nmol) did not induce chromosomal aberrations in vivo. In combination with initiation by 7,12-dimethylbenz[a]anthracene (DMBA) and promotion by RPA, MMS (2 x 100 mumol) turned out to be a rather powerful convertogenic agent ('stage I tumor promoter'). This tumor-inducing efficacy of MMS was synergistically increased by simultaneous application of RPA. These results support the concept that the induction of chromosomal aberrations plays an important role in skin tumor development, i.e. in the conversion stage.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1989

Spondylothoracic dysplasia. Clinical and sonographic diagnosis.

Spondylothoracic dysplasia, also known as short-trunk dwarfism or Jarcho-Levin syndrome, is a fatal autosomal recessive disorder characterized by vertebral and spinal defects with a short thorax. Until recently, in utero diagnosis could only be made radiographically. Sonographic criteria for antenatal diagnosis are discussed in conjunction with a review of the literature.

Abnormalities, Multiple↗
PubMed1989

Diagnosis of adrenal ganglioneuroma in pregnancy with magnetic resonance imaging and ultrasonography. A case report.

A right adrenal gland mass was found during sonographic examination of the right upper quadrant during a workup for hyperemesis gravidarum. Magnetic resonance imaging was used to clarify the origin of the mass. The tumor was nonfunctional. Because of the possibility of a malignancy, the patient underwent a successful second-trimester exploratory laparatomy with right adrenalectomy. Pathology demonstrated a benign ganglioneuroma.

Adrenal Gland Neoplasms↗
PubMed1989

Expression of the kinase domain of mouse protein kinase C in E. coli.

The kinase domain of mouse protein kinase C type alpha has been expressed at high levels in E. coli. The protein has been purified 500-fold taking advantage of the fact that highly expressed fusion proteins precipitate out in the bacterial cell and can be solubilized in 7 M urea. The purified protein can be detected with an antibody generated against a PKC alpha derived synthetic peptide. The purified kinase domain exhibits no measurable kinase activity in a protamin phosphorylation assay. This could be an indication that post-translational modifications of the protein kinase domain which do not happen in bacteria are a requirement for functional enzyme activity or that the regulatory domain of protein kinase C is indispensable for kinase function.

Animals↗
PubMed1988

Molecular cloning of mouse protein kinase C (PKC) cDNA from Swiss 3T3 fibroblasts.

A set of complementary DNAs (cDNAs) that encode the complete 672-amino acid sequence for mouse protein kinase C (PKC) type alpha have been isolated from a mouse Swiss 3T3 cDNA library. Extensive rescreening of this cDNA library only resulted in the isolation of clones of the same PKC species, indicating that Swiss 3T3 fibroblasts express exclusively PKC-alpha. This enzyme is encoded by two different mRNAs that exhibit a substantial heterogeneity in their 3'-noncoding regions. This heterogeneity could have been derived from alternative splicing of the pre-mRNAs or be due to differential usage of the polyadenylation motif. The expression of PKC mRNA in fibroblasts is very low and it is not influenced by treatment with the tumor promoter 12-O-tetradecanoyl-13-phorbol-acetate.

Animals↗
PubMed1988

Effect of tumor promoting phorbol ester TPA on epidermal protein synthesis: stimulation of an elongation factor 2 phosphatase activity by TPA in vivo.

Topical application of the phorbol ester TPA to mouse skin causes an increase in the amount of elongation factor 2 (EF-2), a factor in eukaryotic protein synthesis, in the epidermal cytosol (2- to 3-fold) and particulate fraction (7-fold). Furthermore, as a consequence of this TPA treatment the activity of an epidermal EF-2 phosphatase is stimulated. The EF-2 phosphatase has an apparent molecular weight of around 38,000 daltons. The enzyme activity is induced as early as 45 minutes after TPA treatment and remains at the elevated level for more than 17 hours. Both of the TPA-induced effects result in an increase in unphosphorylated, i.e. active EF-2 and can be suppressed by cyclosporine A.

Animals↗
PubMed1988

The weak immunosuppressant cyclosporine D as well as the immunologically inactive cyclosporine H are potent inhibitors in vivo of phorbol ester TPA-induced biological effects in mouse skin and of Ca2+/calmodulin dependent EF-2 phosphorylation in vitro.

Various biological effects induced by the tumor promoting phorbol ester TPA in mouse skin are comparably suppressed by the immunologically inactive cyclosporine H (CsH) and by the strongly immunosuppressive cyclosporine A (CsA). These effects inhibited include the development of edema, stimulation of alkaline phosphatase activity, DNA and protein synthesis, as well as tumor promotion. Furthermore, CsH, like CsA, inhibits the Ca2+/calmodulin-dependent phosphorylation of the elongation factor 2 (EF-2) in vitro and the TPA-induced increases in the amount of EF-2 in vivo. Similar observations were made using the weak immunosuppressant CsD. We conclude from these results that the ability of cyclosporines to act as immunosuppressants and their ability to inhibit TPA-effects are based on two different mechanisms of action. Inhibition of TPA-effects may involve suppression of calmodulin-dependent processes, such as augmentation and phosphorylation of EF-2.

Alkaline Phosphatase↗
PubMed1988

Effect of diterpene esters on actin cytoskeleton of SV40-transformed keratinocytes is not reproduced by diacylglycerols.

The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) induces a disorganization of the actin cytoskeleton and its redistribution at the periphery of the cells in SV40-transformed human keratinocytes. This phenomenon is induced by other diterpene esters, such as 4-O-methyl TPA, 12-O-ethacrynylphorbol-13-acetate (EPA), 12-O-retinoylphorbol-13-acetate (RPA) and mezerein, which exert either convertogenic or promoting effects in skin tumor development in vivo. Two diacylglycerols: oleyl-acetyl glycerol (OAG) and dioctanoyl-glycerol (DOG) do not induce the disorganization of actin. Thus, the effects of these compounds, as they are found in SV40-transformed human keratinocytes, do not exhibit clear-cut correlations to either their protein kinase C activating abilities, or their effects on different stages of multistage carcinogenesis in mouse skin in vivo.

Actins↗