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Articles 1 - 4 of 4
Full-Text Articles in Life Sciences
Use Of Image Cytometry For Quantification Of Pathogenic Fungi In Association With Host Cells, Charlotte A. Berkes, Leo Li-Ying Chan, Alisha Wilkinson, Benjamin Paradis
Use Of Image Cytometry For Quantification Of Pathogenic Fungi In Association With Host Cells, Charlotte A. Berkes, Leo Li-Ying Chan, Alisha Wilkinson, Benjamin Paradis
Biology Faculty Publications
Studies of the cellular pathogenesis mechanisms of pathogenic yeasts such as Candida albicans, Histoplasma capsulatum, and Cryptococcus neoformans commonly employ infection of mammalian hosts or host cells (i.e. macrophages) followed by yeast quantification using colony forming unit analysis or flow cytometry. While colony forming unit enumeration has been the most commonly used method in the field, this technique has disadvantages and limitations, including slow growth of some fungal species on solid media and low and/or variable plating efficiencies, which is of particular concern when comparing growth of wild-type and mutant strains. Flow cytometry can provide rapid quantitative information regarding yeast …
Myod Synergizes With The E-Protein Heb Beta To Induce Myogenic Differentiation, Maura H. Parker, Robert L.S. Perry, Melanie C. Fauteux, Charlotte A. Berkes, Michael A. Rudnicki
Myod Synergizes With The E-Protein Heb Beta To Induce Myogenic Differentiation, Maura H. Parker, Robert L.S. Perry, Melanie C. Fauteux, Charlotte A. Berkes, Michael A. Rudnicki
Biology Faculty Publications
The MyoD family of basic helix-loop-helix transcription factors function as heterodimers with members of the E-protein family to induce myogenic gene activation. The E-protein HEB is alternatively spliced to generate alpha and beta isoforms. While the function of these molecules has been studied in other cell types, questions persist regarding the molecular functions of HEB proteins in skeletal muscle. Our data demonstrate that HEB alpha expression remains unchanged in both myoblasts and myotubes, whereas HEB beta is upregulated during the early phases of terminal differentiation. Upon induction of differentiation, a MyoD-HEB beta complex bound the E1 E-box of the myogenin …
Myod Targets Chromatin Remodeling Complexes To The Myogenin Locus Prior To Forming A Stable Dna-Bound Complex, Ivana L. De La Serna, Yasuyuki Ohkawa, Charlotte A. Berkes, Donald A. Bergstrom, Caroline S. Dacwag, Stephen J. Tapscott, Anthony N. Imbalzano
Myod Targets Chromatin Remodeling Complexes To The Myogenin Locus Prior To Forming A Stable Dna-Bound Complex, Ivana L. De La Serna, Yasuyuki Ohkawa, Charlotte A. Berkes, Donald A. Bergstrom, Caroline S. Dacwag, Stephen J. Tapscott, Anthony N. Imbalzano
Biology Faculty Publications
The activation of muscle-specific gene expression requires the coordinated action of muscle regulatory proteins and chromatin-remodeling enzymes. Microarray analysis performed in the presence or absence of a dominant-negative BRG1 ATPase demonstrated that approximately one-third of MyoD-induced genes were highly dependent on SWI/SNF enzymes. To understand the mechanism of activation, we performed chromatin immunoprecipitations analyzing the myogenin promoter. We found that H4 hyperacetylation preceded Brg1 binding in a MyoD-dependent manner but that MyoD binding occurred subsequent to H4 modification and Brg1 interaction. In the absence of functional SWI/SNF enzymes, muscle regulatory proteins did not bind to the myogenin promoter, thereby providing …
Mutations In The Non-Helical Linker Segment L1-2 Of Keratin 5 In Patients With Weber-Cockayne Epidermolysis Bullosa Simplex, Yiu-Mo Chan, Qian-Chun Yu, Janine M. Leblanc-Straceski, Angela Christiano, Lena Pulkkinen, Raju S. Kucherlapati, Jouni Uitto, Elaine Fuchs
Mutations In The Non-Helical Linker Segment L1-2 Of Keratin 5 In Patients With Weber-Cockayne Epidermolysis Bullosa Simplex, Yiu-Mo Chan, Qian-Chun Yu, Janine M. Leblanc-Straceski, Angela Christiano, Lena Pulkkinen, Raju S. Kucherlapati, Jouni Uitto, Elaine Fuchs
Biology Faculty Publications
Keratins are the major structural proteins of the epidermis. Analyzing keratin gene sequences, appreciating the switch in keratin gene expression that takes place as epidermal cells commit to terminally differentiate, and elucidating how keratins assemble into 10 nm filaments, have provided the foundation that has led to the discoveries of the genetic bases of two major classes of human skin diseases, epidermolysis bullosa simplex (EBS) and epidermolytic hyperkeratosis (EH). These diseases involve point mutations in either the basal epidermal keratin pair, K5 and K14 (EBS), or the suprabasal pair, K1 and K10 (EH). In severe cases of EBS and EH, …