Biomedical subjects

M F Moran

Publications and source records attributed to M F Moran.

40 records · Page 3Linked to original sources

PubMed1986

DNA repair pathway in alkylated human cells: apurinic/apyrimidinic intermediate resolved by Escherichia coli endonuclease IV-coupled alkaline elution.

Apurinic/apyrimidinic (AP) sites were measured in HeLa cells by digestion of cellular DNA with Escherichia coli endonuclease IV, an AP-specific endonuclease, prior to alkaline elution. The absence of non-specific endonuclease activity allowed endonuclease IV-sensitive AP sites to be detected with the sensitivity of conventional alkaline elution. Cells that were alkylated with dimethyl sulfate contained AP sites that were repaired along with DNA single-strand breaks during a post-alkylation recovery period. These results show that DNA alkylation products are repaired, at least in part, via an AP intermediate suggesting a repair pathway initiated by DNA glycosylases followed by DNA incision by AP endonuclease.

Alkylation↗

PubMed1985

Inhibition of poly(ADP-ribose)polymerase causes increased DNA strand breaks without decreasing strand rejoining in alkylated HeLa cells.

Treatment of alkylated HeLa cells with 3-aminobenzamide, an inhibitor of poly(ADP-ribose) polymerase, increased the number of DNA strand breaks but did not affect the rate of strand rejoining. This suggests that an increase in DNA incision, not a decrease in ligation, results from the inhibition of poly(ADP-ribose) polymerase in cells recovering from DNA damaged by alkylating agents.

Alkylation↗

PubMed1976

Upper respiratory problems in the yellow nail syndrome.

A case of the Yellow Nail Syndrome is described. The characteristic nail changes were associated with pleural effusions, lymphoedema of the face and legs and upper respiratory symptoms. The finding of extremely hard ear wax has not been reported previously. A satisfactory response to combination diuretic therapy was seen. The case of recognition of the Syndrome is emphasized together with the danger of excessive investigation if the nails are not inspected. Possible mechanisms for the formation of extremely hard cerumen are discussed.

Hearing Disorders↗

PubMedDate not supplied

The exchange factor Ras-GRF2 activates Ras-dependent and Rac-dependent mitogen-activated protein kinase pathways.

Ras and Rac are membrane-associated GTPases that function as molecular switches activating intracellular mitogen-activated protein kinase (MAPK) cascades and other effector pathways in response to extracellular signals [1]. Activation of Ras and Rac into their GTP-bound conformations is directly controlled by specific guanine-nucleotide exchange factors (GEFs), which catalyze GDP release. Several Ras-specific GEFs that are related to the budding yeast protein Cdc25p have been described, whereas GEFs for Rac-related GTPases contain a region that is homologous to the oncoprotein DbI [2-3]. The Ras-GRF1 and Ras-GRF2 proteins, which couple Ras activation to serpentine receptors and calcium signals, contain both Cdc25 and DbI homology (DH) regions [3-4]. Here, we demonstrate that Ras-GRF2 is a bifunctional signaling protein that is able to bind and activate Ras and Rac, and thereby coordinate the activation of the extracellular-signal-regulated kinase (ERK) and stress-activated protein kinase (SAPK) pathways.

Anisomycin↗