scholarly journals The GA-binding Protein Can Serve as Both an Activator and Repressor ofribosomal proteinGene Transcription

1996 ◽  
Vol 271 (8) ◽  
pp. 4388-4395 ◽  
Author(s):  
R. Robert Genuario ◽  
Robert P. Perry
Keyword(s):  
Binding Protein ◽  
Ga Binding Protein

scholarly journals GA-Binding Protein Is Dispensable for Neuromuscular Synapse Formation and Synapse-Specific Gene Expression

2007 ◽  
Vol 27 (13) ◽  
pp. 5040-5046 ◽  
Author(s):  
Alexander Jaworski ◽  
Cynthia L. Smith ◽  
Steven J. Burden
Keyword(s):  
Gene Expression ◽  
Synapse Formation ◽  
Binding Protein ◽  
Neuromuscular Synapse ◽  
Specific Gene ◽  
Promoter Regions ◽  
Specific Gene Expression ◽  
Muscle Gene Expression ◽  
Synaptic Region ◽  
Ga Binding Protein

ABSTRACT The mRNAs encoding postsynaptic components at the neuromuscular junction are concentrated in the synaptic region of muscle fibers. Accumulation of these RNAs in the synaptic region is mediated, at least in part, by selective transcription of the corresponding genes in synaptic myofiber nuclei. The transcriptional mechanisms that are responsible for synapse-specific gene expression are largely unknown, but an Ets site in the promoter regions of acetylcholine receptor (AChR) subunit genes and other “synaptic” genes is required for synapse-specific transcription. The Ets domain transcription factor GA-binding protein (GABP) has been implicated to mediate synapse-specific gene expression. Inactivation of GABPα, the DNA-binding subunit of GABP, leads to early embryonic lethality, preventing analysis of synapse formation in gabpα mutant mice. To study the role of GABP at neuromuscular synapses, we conditionally inactivated gabpα in skeletal muscle and studied synaptic differentiation and muscle gene expression. Although expression of rb, a target of GABP, is elevated in muscle tissue deficient in GABPα, clustering of synaptic AChRs at synapses and synapse-specific gene expression are normal in these mice. These data indicate that GABP is dispensable for synapse-specific transcription and maintenance of normal AChR expression at synapses.

scholarly journals Redox Regulation of GA-binding Protein-α DNA Binding Activity

1996 ◽  
Vol 271 (41) ◽  
pp. 25617-25623 ◽  
Author(s):  
Mark E. Martin ◽  
Yurii Chinenov ◽  
Mi Yu ◽  
Tonya K. Schmidt ◽  
Xiu-Ying Yang
Keyword(s):  
Dna Binding ◽  
Redox Regulation ◽  
Binding Protein ◽  
Binding Activity ◽  
Dna Binding Activity ◽  
Ga Binding Protein

scholarly journals GA binding protein augments autophagy via transcriptional activation ofBECN1-PIK3C3complex genes

Autophagy ◽  
2014 ◽  
Vol 10 (9) ◽  
pp. 1622-1636 ◽  
Author(s):  
Wan Zhu ◽  
Gayathri Swaminathan ◽  
Edward D Plowey
Keyword(s):  
Transcriptional Activation ◽  
Binding Protein ◽  
Ga Binding Protein

scholarly journals GA-binding protein GABPβ1 is required for the proliferation of neural stem/progenitor cells

2019 ◽  
Vol 39 ◽  
pp. 101501 ◽  
Author(s):  
Cong Liu ◽  
Shang-Kun Dai ◽  
Zhen Sun ◽  
Zhuo Wang ◽  
Pei-Pei Liu ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Binding Protein ◽  
Neural Stem Progenitor Cells ◽  
Ga Binding Protein

scholarly journals Activation of Utrophin Promoter by Heregulin via theets-related Transcription Factor Complex GA-binding Protein α/β

1999 ◽  
Vol 10 (6) ◽  
pp. 2075-2086 ◽  
Author(s):  
Tejvir S. Khurana ◽  
Alan G. Rosmarin ◽  
Jing Shang ◽  
Thomas O. B. Krag ◽  
Saumya Das ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Transcription Factors ◽  
Neuromuscular Junction ◽  
Muscle Cell ◽  
Cell Cultures ◽  
Binding Protein ◽  
Duchenne's Muscular Dystrophy ◽  
Ga Binding Protein

Utrophin/dystrophin-related protein is the autosomal homologue of the chromosome X-encoded dystrophin protein. In adult skeletal muscle, utrophin is highly enriched at the neuromuscular junction. However, the molecular mechanisms underlying regulation of utrophin gene expression are yet to be defined. Here we demonstrate that the growth factor heregulin increases de novo utrophin transcription in muscle cell cultures. Using mutant reporter constructs of the utrophin promoter, we define the N-box region of the promoter as critical for heregulin-mediated activation. Using this region of the utrophin promoter for DNA affinity purification, immunoblots, in vitro kinase assays, electrophoretic mobility shift assays, and in vitro expression in cultured muscle cells, we demonstrate thatets-related GA-binding protein α/β transcription factors are activators of the utrophin promoter. Taken together, these results suggest that the GA-binding protein α/β complex of transcription factors binds and activates the utrophin promoter in response to heregulin-activated extracellular signal–regulated kinase in muscle cell cultures. These findings suggest methods for achieving utrophin up-regulation in Duchenne’s muscular dystrophy as well as mechanisms by which neurite-derived growth factors such as heregulin may influence the regulation of utrophin gene expression and subsequent enrichment at the neuromuscular junction of skeletal muscle.

scholarly journals Transcriptional Regulation of Fas Gene Expression by GA-binding Protein and AP-1 in T Cell Antigen Receptor·CD3 Complex-stimulated T Cells

1999 ◽  
Vol 274 (49) ◽  
pp. 35203-35210 ◽  
Author(s):  
Xiao Rui Li ◽  
Anita S.-F. Chong ◽  
Jianming Wu ◽  
Kenneth A. Roebuck ◽  
Aseem Kumar ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Transcriptional Regulation ◽  
T Cell ◽  
Binding Protein ◽  
Cell Antigen ◽  
Ga Binding Protein

scholarly journals Induction of utrophin gene expression by heregulin in skeletal muscle cells: Role of the N-box motif and GA binding protein

1999 ◽  
Vol 96 (6) ◽  
pp. 3223-3227 ◽  
Author(s):  
A. O. Gramolini ◽  
L. M. Angus ◽  
L. Schaeffer ◽  
E. A. Burton ◽  
J. M. Tinsley ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Binding Protein ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Ga Binding Protein

scholarly journals Targeting the GA Binding Protein β1L Isoform Does Not Perturb Lymphocyte Development and Function

2008 ◽  
Vol 28 (13) ◽  
pp. 4300-4309 ◽  
Author(s):  
Hai-Hui Xue ◽  
Xuefang Jing ◽  
Julie Bollenbacher-Reilley ◽  
Dong-Mei Zhao ◽  
Jodie S. Haring ◽  
...  
Keyword(s):  
B Cells ◽  
Target Genes ◽  
Splice Variants ◽  
Binding Protein ◽  
Critical Role ◽  
Dominant Negative ◽  
T And B Cells ◽  
Carboxy Terminal ◽  
And Function ◽  
Ga Binding Protein

ABSTRACT GA binding protein (GABP) is a ubiquitously expressed Ets family transcription factor that consists of two subunits, GABPα and GABPβ. GABPα binds to DNA, and GABPβ heterodimerizes with GABPα and possesses the ability to transactivate target genes. Our previous studies using GABPα-deficient mice revealed that GABPα is required for the development of both T and B cells. Two splice variants of GABPβ are generated from the Gabpb1 locus and differ in their carboxy-terminal lengths and sequences. The longer isoform (GABPβ1L) can homodimerize and thus form α2β2 tetramers depending on the gene context, whereas the shorter isoform (GABPβ1S) cannot. In this study, we generated mice that are deficient in GABPβ1L but that retain the expression of GABPβ1S. Surprisingly, GABPβ1L−/− mice had normal T- and B-cell development, and mature T and B cells showed normal responses to various stimuli. In contrast, targeting both GABPβ1L and GABPβ1S resulted in early embryonic lethality. Because of its incapability of forming homodimers, GABPβ1S has been suspected to have a dominant negative role in regulating GABP target genes. Our findings argue against such a possibility and rather suggest that GABPβ1S has a critical role in maintaining the transcriptional activity of the GABPα/β complex.

Abstract 3387: Upregulation of gene expression in oligodendrogliomas is linked to an increase in GA binding protein alpha transcription

2014 ◽  
Author(s):  
Barbara Klink ◽  
Karol Szafranski ◽  
Jaime Campos-Valenzuela ◽  
Sophie Eisenreich ◽  
Dietmar Krex ◽  
...  
Keyword(s):  
Gene Expression ◽  
Binding Protein ◽  
Ga Binding Protein
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