scholarly journals Cell type-specific filamin complex regulation by a novel class of HECT ubiquitin ligase is required for normal cell motility and patterning

Development ◽  
2011 ◽  
Vol 138 (8) ◽  
pp. 1583-1593 ◽  
Author(s):  
S. L. Blagg ◽  
S. E. Battom ◽  
S. J. Annesley ◽  
T. Keller ◽  
K. Parkinson ◽  
...  
Keyword(s):  
Cell Motility ◽  
Ubiquitin Ligase ◽  
Normal Cell ◽  
Cell Type ◽  
Cell Type Specific ◽  
Complex Regulation

scholarly journals Cell type-specific filamin complex regulation by a novel class of HECT ubiquitin ligase is required for normal cell motility and patterning

2011 ◽  
Vol 124 (8) ◽  
pp. e1-e1
Author(s):  
S. L. Blagg ◽  
S. E. Battom ◽  
S. J. Annesley ◽  
T. Keller ◽  
K. Parkinson ◽  
...  
Keyword(s):  
Cell Motility ◽  
Ubiquitin Ligase ◽  
Normal Cell ◽  
Cell Type ◽  
Cell Type Specific ◽  
Complex Regulation

scholarly journals Spatiotemporal dynamics of SETD5-containing NCoR–HDAC3 complex determines enhancer activation for adipogenesis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yoshihiro Matsumura ◽  
Ryo Ito ◽  
Ayumu Yajima ◽  
Rei Yamaguchi ◽  
Toshiya Tanaka ◽  
...  
Keyword(s):  
Gene Expression ◽  
Histone Acetylation ◽  
Ubiquitin Ligase ◽  
Cellular Differentiation ◽  
Specific Gene ◽  
Cell Type ◽  
Set Domain ◽  
Protein Levels ◽  
Primed State ◽  
Cell Type Specific

AbstractEnhancer activation is essential for cell-type specific gene expression during cellular differentiation, however, how enhancers transition from a hypoacetylated “primed” state to a hyperacetylated-active state is incompletely understood. Here, we show SET domain-containing 5 (SETD5) forms a complex with NCoR-HDAC3 co-repressor that prevents histone acetylation of enhancers for two master adipogenic regulatory genes Cebpa and Pparg early during adipogenesis. The loss of SETD5 from the complex is followed by enhancer hyperacetylation. SETD5 protein levels were transiently increased and rapidly degraded prior to enhancer activation providing a mechanism for the loss of SETD5 during the transition. We show that induction of the CDC20 co-activator of the ubiquitin ligase leads to APC/C mediated degradation of SETD5 during the transition and this operates as a molecular switch that facilitates adipogenesis.

The Protein 4.1 Tumor Suppressor, DAL-1, Impairs Cell Motility, But Regulates Proliferation in a Cell-Type-Specific Fashion

2001 ◽  
Vol 8 (2) ◽  
pp. 266-278 ◽  
Author(s):  
David H. Gutmann ◽  
Angela C. Hirbe ◽  
Zhi-yong Huang ◽  
Carrie A. Haipek
Keyword(s):  
Tumor Suppressor ◽  
Cell Motility ◽  
Cell Type ◽  
Protein 4.1 ◽  
A Cell ◽  
Cell Type Specific

Spatiotemporal dynamics of SETD5-containing NCoR-HDAC3 complex determines enhancer activation for adipogenesis

2021 ◽  
Author(s):  
Yoshihiro Matsumura ◽  
Ryo Ito ◽  
Ayumu Yajima ◽  
Rei Yamaguchi ◽  
Kenta Magoori ◽  
...  
Keyword(s):  
Gene Expression ◽  
Histone Acetylation ◽  
Ubiquitin Ligase ◽  
Cellular Differentiation ◽  
Specific Gene ◽  
Cell Type ◽  
Set Domain ◽  
Protein Levels ◽  
Primed State ◽  
Cell Type Specific

Abstract Enhancer activation is essential for cell-type specific gene expression during cellular differentiation, however, how enhancers transition from a hypoacetylated “primed” state to a hyperacetylated-active state is incompletely understood. Here, we show SET domain-containing 5 (SETD5) forms a complex with NCoR-HDAC3 co-repressor that prevents histone acetylation of enhancers for two master adipogenic regulatory genes Cebpa and Pparg early during adipogenesis. The loss of SETD5 from the complex is followed by enhancer hyperacetylation. SETD5 protein levels were transiently increased and rapidly degraded prior to enhancer activation providing a mechanism for the loss of SETD5 during the transition. We show that induction of the CDC20 co-activator of the ubiquitin ligase leads to APC/C mediated degradation of SETD5 during the transition and this operates as a molecular switch that facilitates adipogenesis.

scholarly journals IQGAP1 in Podosome /Invadosome is Involved in the Progression of Glioblastoma Multiforme Depending on the Tumor Status

2016 ◽  
Author(s):  
Deborah Rotoli ◽  
Natalia Pérez-Rodríguez ◽  
Manuel Morales ◽  
María Del Carmen Maeso ◽  
Julio Ávila ◽  
...  
Keyword(s):  
Glioblastoma Multiforme ◽  
Normal Cell ◽  
Primary Brain Tumor ◽  
Cell Physiology ◽  
Positive Staining ◽  
Cell Type ◽  
Cellular Functions ◽  
Tissue Samples ◽  
Cell Type Specific ◽  
Human Gbm

Glioblastoma multiforme (GBM) is the most frequent and aggressive primary brain tumor. GBM is formed by a very heterogeneous astrocyte population, neurons, neovascularization and infiltrating myeloid cells (microglia and monocyte derived macrophages). The IQGAP1 scaffold protein interacts with components of the cytoskeleton, cell adhesion molecules, and several signaling molecules to regulate cell morphology and motility, cell cycle and other cellular functions. IQGAP1 overexpression and delocalization has been observed in several tumors, suggesting a role for this protein in cell proliferation, transformation and invasion. IQGAP1 has been identified as a marker of amplifying cancer cells in GBMs. To determine the involvement of IQGAP1 in the onco-biology of GBM, we performed immunohistochemical confocal microscopical analysis of the IQGAP1 protein in human GBM tissue samples using cell type-specific markers. IQGAP1 immunostaining and subcellular localization was heterogeneous; the protein was located in the plasma membrane and, at variable levels, in nucleus and/or cytosol). Moreover, IQGAP1 positive staining was found in podosome/invadopodia-like structures. IQGAP1+ staining was observed in neurons (Map2+ cells), in cancer stem cells (CSC; nestin+) and in several macrophages (CD31+ or Iba1+). Our results indicate that the IQGAP1 protein is involved in normal cell physiology and also in oncologic processes.

IFIH1-deficiency results in a cell-type specific alteration of autophagic activity in response to S. typhimurium

2017 ◽  
Vol 55 (05) ◽  
pp. e28-e56
Author(s):  
S Macheiner ◽  
R Gerner ◽  
A Pfister ◽  
A Moschen ◽  
H Tilg
Keyword(s):  
Cell Type ◽  
A Cell ◽  
Cell Type Specific ◽  
Autophagic Activity ◽  
Specific Alteration

Cell Type–Specific Transcriptional and Epigenetic Profiles from a Rare Neuronal Population within the Arcuate Nucleus

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2430-PUB
Author(s):  
FRANKIE D. HEYWARD ◽  
EVAN ROSEN
Keyword(s):  
Arcuate Nucleus ◽  
Neuronal Population ◽  
Cell Type ◽  
Cell Type Specific
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