View additional product information for MEM - Citations (11095072, 11095080, 11095114, 11095098)
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Abstract
Two adaptor proteins differentially modulate the phosphorylation and biophysics of kv1.3 ion channel by SRC kinase.
Authors Cook Karen K; Fadool Debra A;
JournalJ Biol Chem
PubMed ID11812778
'The Shaker family K(+) channel protein, Kv1.3, is tyrosine phosphorylated by v-Src kinase at Tyr(137) and Tyr(449) to modulate current magnitude and kinetic properties. Despite two proline rich sequences and these phosphotyrosines contained in the carboxyl and amino terminals of the channel, v-Src kinase fails to co-immunoprecipitate with Kv1.3 as ... More
Dependence of selective gene activation on the androgen receptor NH2- and COOH-terminal interaction.
Authors He Bin; Lee Lori W; Minges John T; Wilson Elizabeth M;
JournalJ Biol Chem
PubMed ID12000757
'The agonist-induced androgen receptor NH(2)- and COOH-terminal (N/C) interaction is mediated by the FXXLF and WXXLF NH(2)-terminal motifs. Here we demonstrate that agonist-dependent transactivation of prostate-specific antigen (PSA) and probasin enhancer/promoter regions requires the N/C interaction, whereas the sex-limited protein gene and mouse mammary tumor virus long terminal repeat do ... More
Acute hippocampal slice preparation and hippocampal slice cultures.
AuthorsLein PJ, Barnhart CD, Pessah IN
JournalMethods Mol Biol
PubMed ID21815062
'A major advantage of hippocampal slice preparations is that the cytoarchitecture and synaptic circuits of the hippocampus are largely retained. In neurotoxicology research, organotypic hippocampal slices have mostly been used as acute ex vivo preparations for investigating the effects of neurotoxic chemicals on synaptic function. More recently, hippocampal slice cultures, ... More
The Discodermia calyx toxin calyculin a enhances cyclin D1 phosphorylation and degradation, and arrests cell cycle progression in human breast cancer cells.
AuthorsEdelson JR, Brautigan DL
JournalToxins (Basel)
PubMed ID22069692
'Cyclin D1 is a key regulator of the cell cycle that is over expressed in more than half of breast cancer patients. The levels of cyclin D1 are controlled primarily through post-translational mechanisms and phosphorylation of cyclin D1 at T286 induces its proteasomal degradation. To date, no studies have explored ... More