A5081621005- DNA and Nucleic Acid Chemistry
- Pancreatic function and diabetes
- DNA Repair Mechanisms
- Metabolism, Diabetes, and Cancer
- Microtubule and mitosis dynamics
- Immune Cell Function and Interaction
- RNA and protein synthesis mechanisms
- Genomics and Chromatin Dynamics
- Growth Hormone and Insulin-like Growth Factors
- Epigenetics and DNA Methylation
- Cancer-related Molecular Pathways
- CRISPR and Genetic Engineering
- RNA Research and Splicing
- Cancer-related gene regulation
- T-cell and B-cell Immunology
- Genetics, Bioinformatics, and Biomedical Research
- Bacteriophages and microbial interactions
- Monoclonal and Polyclonal Antibodies Research
- Cardiomyopathy and Myosin Studies
- Plant Genetic and Mutation Studies
- Immune cells in cancer
- Virology and Viral Diseases
- NF-κB Signaling Pathways
- Birth, Development, and Health
- Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
Duke University
1990-2023
Duke University Hospital
1991-2017
Duke Medical Center
1991-2017
Duke Cancer Institute
2015-2017
Emory University
1984-1992
DNA double-strand breaks (DSBs) are traditionally associated with cancer through their abilities to cause chromosomal instabilities or gene mutations. Here we report a new class of self-inflicted DSBs that can drive tumor growth irrespective effects on genomic stability. We discover mechanism which cells in own genome spontaneously independent reactive oxygen species replication stress. In this mechanism, low-level cytochrome c leakage from the mitochondria leads sublethal activation...
The gene for CD59 [membrane inhibitor of reactive lysis (MIRL), protectin], a phosphatidylinositol-linked surface glycoprotein that regulates the formation polymeric C9 complex complement and is deficient on abnormal hematopoietic cells patients with paroxysmal nocturnal hemoglobinuria, consists four exons spanning 20 kilobases. untranslated first exon preceded by G+C-rich promoter region lacks consensus TATA or CAAT motif. second encodes hydrophobic leader sequence protein, third...
GH and PRL stimulate insulin production in pancreatic β-cells through induction of gene transcription. The transcriptional effects are mediated the binding signal transducer activator transcription-5 (STAT5) to a consensus recognition sequence (TTCnnnGAA) rat insulin-1 promoter. In this study we demonstrate that also induces STAT5 proteins motif. However, magnitude nuclear proteins, as assessed by electrophoretic mobility shift assays, was only 1/30th same theβ -casein site. differences...
Previous studies have shown that lactogenic hormones stimulate beta-cell proliferation and insulin production in pancreatic islets. However, all such been conducted cells incubated medium containing glucose. Since glucose independently stimulates replication production, it is unclear whether the effects of prolactin (PRL) on gene expression are exerted directly or through uptake and/or metabolism We examined interactions between PRL regulation transcription transporter-2 (glut-2) glucokinase...
To delineate the roles of lactogens and GH in control perinatal postnatal growth, fat deposition, insulin production, action, we generated a novel mouse model that combines resistance to all lactogenic hormones with severe deficiency pituitary GH. The was created by breeding PRL receptor (PRLR)-deficient (knockout) males GH-deficient (little) females. In contrast mice isolated or PRLR deficiencies, double-mutant (lactogen-resistant GH-deficient) on d 7 life had growth failure hypoglycemia....
The human CD7 molecule is a 40-kDa member of the immunoglobulin gene superfamily that expressed on T-lymphoid and myeloid precursors in fetal liver bone marrow. also T lymphocytes multiple stages T-cell development, including major subset mature peripheral cells. In this paper we report isolation characterization 5' flanking region. Sequence analysis revealed comprises four exons span 3.5 kilobases. region (506 base pairs) has high G + C content no "TATA" or "CCAAT" elements. DNase I...
Prolactin (PRL) induces β-cell proliferation and glucose-stimulated insulin secretion (GSIS) counteracts the effects of glucocorticoids on production. The mechanisms by which PRL up-regulates GSIS are unknown. We used rat islets insulinoma (INS-1) cells to explore interactions PRL, glucose, dexamethasone (DEX) in regulation pyruvate carboxylase (PC), dehydrogenase (PDH), kinases (PDKs), catalyze phosphorylation inactivation PDH. increased 37% (P < 0.001) islets. Glucose at...
The mechanisms by which lactogenic hormones promote β-cell expansion remain poorly understood. Because prolactin (PRL) up-regulates glucose transporter 2, glucokinase, and pyruvate dehydrogenase activities, we reasoned that availability might mediate or modulate the effects of PRL on mass. Here, used male rat islets to show have differential but complementary expression cell cyclins, cycle inhibitors, various other genes known regulate replication, including insulin receptor substrate...
Journal Article Avian tropomyosin gene expression Get access Gary J. Lindquester, Lindquester * Emory University, Biology DepartmentAtlanta, GA 30322, USA + Present address: Rhodes College, 2000 North Parkway, Memphis, TN 38112, To whom correspondence should be addressed Search for other works by this author on: Oxford Academic PubMed Google Scholar James E. Flach, Flach § Department of Biology, Yale New Haven, CT, Donald Fleenor, Fleenor φ Medicine, Duke Durham, NC, Kathryn H. Hickman,...
Altered cellular responses to DNA damage can contribute cancer development, progression, and therapeutic resistance. Mutations in key response factors occur across many types, the damage-responsive gene, TP53, is frequently mutated a high percentage of cancers. We recently reported that an alternative splicing pathway induced by regulates TP53 RNA further modulates stress responses. Through damage-induced inhibition SMG1 kinase, pre-mRNA alternatively spliced generate TP53b mRNA p53b protein...
Journal Article Analysis of xanthine dehydrogensse mRNA levels in mutants affecting the expression rosy locus Get access M. Covington, Covington Department Biology, Emory UniversityAtlanta, GA 30322, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar D. Fleenor, Fleenor R.B. Devlin Nucleic Acids Research, Volume 12, Issue 11, 11 June 1984, Pages 4559–4573, https://doi.org/10.1093/nar/12.11.4559 Published: 1984 history Received: 28 November 1983 Revision...
Multiple members of the cohesin complex are involved in regulation DNA replication and transcription vicinity double-strand breaks their role(s) regulated by ATM kinase.
CD7 is a 40-kDa transmembrane glycoprotein member of the lg gene superfamily expressed on most peripheral blood T lymphocytes and NK cells. also myeloid, NK, B, cell precursors during adult hematopoiesis. Because Thy-1 absent in human thymocytes cells shows structural similarities to gene, we have suggested that may be functional homologue humans mouse Thy-1. To study tissue-specific expression utilizing its own promoter, constructed transgenic mice contained both coding flanking regions...
Abstract Much of our understanding the mechanisms involved in cellular DNA damage response pathways have come from studies human cancer susceptibility syndromes. ATM, gene mutated cancer-prone, radiosensitive disorder, Ataxia-telangiectasia (A-T), is a protein kinase that central mediator responses to double strand breaks cells. Once activated, ATM phosphorylates numerous substrates cell modulate cell's damage. p53, one many targets kinase, critical cycle changes and death signaling...
<p>S1. Identification of novel ATM-interactors using BioID. S2.NIPBL, PDS5A, and PDS5B are required for chromosomal stability viability after IR. S3. Mutation Fok1 nuclease domain blocks DSB formation. S4. Low dose IR causes suppression DNA replication within the vicinity DSBs. S5. Fok1-induced DSBs do not result in a decrease nuclear replication. S6. Repression around is dependent on ATM ATR or DNAPK. S7. phosphorylation cohesin repression DSB.</p>
<p>Supplemental Figure Legends 1-7</p>