Publications by authors named "Audra M Foshage"
Perturbations in insulin/IGF signaling and manganese (Mn) uptake and signaling have been separately reported in Huntington's disease (HD) models. Insulin/IGF supplementation ameliorates HD phenotypes via upregulation of AKT, a known Mn-responsive kinase. Limited evidence both in vivo and in purified biochemical systems suggest Mn enhances insulin/IGF receptor (IR/IGFR), an upstream tyrosine kinase of AKT.
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- The study investigates how mutations in the Huntingtin (Htt) gene affect autophagy, a cellular process important for clearing damaged proteins, in Huntington's disease (HD) models.
- It finds that low levels of manganese (Mn), a crucial metal for cellular function, lead to impaired autophagy in HD cells, while acute exposure to Mn can stimulate the formation of autophagosomes.
- Restoration of Mn levels helps correct a specific autophagic defect in HD cells, suggesting that improving Mn bioavailability could potentially restore autophagic function and aid in clearing harmful protein aggregates associated with the disease.
Article Synopsis
- WDR5, a protein associated with chromatin, is a potential target for cancer treatment, focusing on inhibiting a specific area known as the "WIN site."
- Researchers have created effective WIN site inhibitors that demonstrate how WDR5 interacts with chromatin and affects specific gene expressions.
- These inhibitors can remove WDR5 from chromatin, leading to decreased gene expression and potential therapeutic implications for various types of cancer.
The MYC oncogenes encode a family of transcription factors that feature prominently in cancer. MYC proteins are overexpressed or deregulated in a majority of malignancies and drive tumorigenesis by inducing widespread transcriptional reprogramming that promotes cell proliferation, metabolism, and genomic instability. The ability of MYC to regulate transcription depends on its dimerization with MAX, which creates a DNA-binding domain that recognizes specific sequences in the regulatory elements of MYC target genes.
View Article and Find Full Text PDFMYC is an oncoprotein transcription factor that is overexpressed in the majority of malignancies. The oncogenic potential of MYC stems from its ability to bind regulatory sequences in thousands of target genes, which depends on interaction of MYC with its obligate partner, MAX. Here, we show that broad association of MYC with chromatin also depends on interaction with the WD40-repeat protein WDR5.
View Article and Find Full Text PDFActivation of kappa-opioid receptors (KORs) in monoamine circuits results in dysphoria-like behaviors and stress-induced reinstatement of drug seeking in both conditioned place preference (CPP) and self-administration models. Noradrenergic (NA) receptor systems have also been implicated in similar behaviors. Dynorphinergic projections terminate within the locus coeruleus (LC), a primary source of norepinephrine in the forebrain, suggesting a possible link between the NA and dynorphin/kappa opioid systems, yet the implications of these putative interactions have not been investigated.
View Article and Find Full Text PDFBackground: The Transient Receptor Potential (TRP) ion channel TRPA1 is a key player in pain pathways. Irritant chemicals activate ion channel TRPA1 via covalent modification of N-terminal cysteines. We and others have shown that 15-Deoxy-Δ12, 14-prostaglandin J2 (15d-PGJ2) similarly activates TRPA1 and causes channel-dependent nociception.
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