scholarly journals Improved Knockout Methodology Reveals That Frog Virus 3 Mutants Lacking either the 18K Immediate-Early Gene or the Truncated vIF-2  Gene Are Defective for Replication and Growth In Vivo

2011 ◽  
Vol 85 (21) ◽  
pp. 11131-11138 ◽  
Author(s):  
G. Chen ◽  
B. M. Ward ◽  
K. H. Yu ◽  
V. G. Chinchar ◽  
J. Robert
Keyword(s):  
Immediate Early Gene ◽  
Early Gene ◽  
Immediate Early ◽  
Frog Virus 3 ◽  
Frog Virus

scholarly journals Circadian regulation of the immediate early gene Neuronal Pentraxin 2 secretion: in vivo imaging study

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S275
Author(s):  
Seung-Eon Roh ◽  
Meifang Xiao ◽  
Jiechao Zhuo ◽  
Alena Savonenko ◽  
Paul Worley
Keyword(s):  
In Vivo Imaging ◽  
Imaging Study ◽  
Immediate Early Gene ◽  
Early Gene ◽  
Immediate Early ◽  
Circadian Regulation ◽  
Neuronal Pentraxin

Expression of zebrafish goosecoid and no tail gene products in wild-type and mutant no tail embryos

Development ◽  
1994 ◽  
Vol 120 (4) ◽  
pp. 843-852 ◽  
Author(s):  
S. Schulte-Merker ◽  
M. Hammerschmidt ◽  
D. Beuchle ◽  
K.W. Cho ◽  
E.M. De Robertis ◽  
...  
Keyword(s):  
Early Stage ◽  
Immediate Early Gene ◽  
Dorsal Side ◽  
Early Gene ◽  
Immediate Early ◽  
Direct Role ◽  
Midblastula Transition ◽  
No Tail ◽  
In Cells

goosecoid is an immediate early gene expressed at the dorsal blastoporal lip of the Xenopus gastrula. Microinjection experiments have suggested a direct role for goosecoid in organizing the dorsoventral axis of the frog embryo. Here we characterize the zebrafish homologue of goosecoid (gsc) and compare its expression to that of Brachyury or no tail (ntl), another immediate early gene required in developing mesoderm. We show that gsc exhibits two independent phases of expression: an early one in cells anterior to the presumptive notochord, but not in cells of the notochord itself, and a later one in neural crest derivatives in the larval head. Zygotic gsc transcripts are detected soon after the midblastula transition, and at the blastula stage form a gradient with a maximum at the dorsal side. Use of gsc as a dorsal marker allowed us to demonstrate that ntl expression is initially activated at the dorsal side of the blastula. At this early stage, gsc and ntl show overlapping domains of expression and are co-expressed in cells at the dorsal midline of the early gastrula. However, gsc- and ntl-expressing cells become separated in the course of gastrulation, with gsc being expressed in the axial hypoblast (prechordal plate) anterior to the ntl-expressing presumptive notochord cells. Studies with mutant embryos suggest that gsc is independent of ntl function in vivo.

In vivo carbon monoxide exposure and hypoxic hypoxia stimulate immediate early gene expression

1997 ◽  
Vol 434 (5) ◽  
pp. 568-574 ◽  
Author(s):  
Bernhard Gess ◽  
Konrad Wolf ◽  
Michael Pfeifer ◽  
Günter A. J. Riegger ◽  
A. Kurtz
Keyword(s):  
Gene Expression ◽  
Carbon Monoxide ◽  
Immediate Early Gene ◽  
Hypoxic Hypoxia ◽  
Early Gene ◽  
Immediate Early ◽  
Early Gene Expression

scholarly journals Protein Kinase Cδ Blocks Immediate-Early Gene Expression in Senescent Cells by Inactivating Serum Response Factor

2004 ◽  
Vol 24 (16) ◽  
pp. 7298-7311 ◽  
Author(s):  
Keith Wheaton ◽  
Karl Riabowol
Keyword(s):  
Gene Expression ◽  
Protein Kinase ◽  
Serum Response Factor ◽  
Immediate Early Gene ◽  
Early Gene ◽  
Immediate Early ◽  
Response Factor ◽  
Serum Response

ABSTRACT Fibroblasts lose the ability to replicate in response to growth factors and become unable to express growth-associated immediate-early genes, including c-fos and egr-1, as they become senescent. The serum response factor (SRF), a major transcriptional activator of immediate-early gene promoters, loses the ability to bind to the serum response element (SRE) and becomes hyperphosphorylated in senescent cells. We identify protein kinase C delta (PKCδ) as the kinase responsible for inactivation of SRF both in vitro and endogenously in senescent cells. This is due to a higher level of PKCδ activity as cells age, production of the PKCδ catalytic fragment, and its nuclear localization in senescent but not in low-passage-number cells. The phosphorylation of T160 of SRF by PKCδ in vitro and in vivo led to loss of SRF DNA binding activity. Both the PKCδ inhibitor rottlerin and ectopic expression of a dominant negative form of PKCδ independently restored SRE-dependent transcription and immediate-early gene expression in senescent cells. Modulation of PKCδ activity in vivo with rottlerin or bistratene A altered senescent- and young-cell morphology, respectively. These observations support the idea that the coordinate transcriptional inhibition of several growth-associated genes by PKCδ contributes to the senescent phenotype.

scholarly journals Sleep deprivation rapidly upregulates serotonin 2A receptor expression via the immediate early gene Egr3

2019 ◽  
Author(s):  
X. Zhao ◽  
K. T. Meyers ◽  
A. McBride ◽  
K. K. Marballi ◽  
A. M. Maple ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Immediate Early Gene ◽  
Receptor Expression ◽  
Early Gene ◽  
Immediate Early ◽  
Early Growth Response ◽  
Brain Receptor ◽  
Serotonin 2A

AbstractSerotonin 2A receptors (5-HT2ARs) mediate the effects of hallucinogenic drugs and antipsychotic medications, and are reduced in schizophrenia patients’ brains. However, the mechanisms that regulate 5-HT2AR expression remain poorly understood. We show that an environmental stimulus, sleep deprivation, upregulates 5-HT2ARs in the mouse frontal cortex (FC) in just 6-8 hours. This induction requires the immediate early gene transcription factor early growth response 3 (Egr3). Further, EGR3 binds to the Htr2a promoter in the FC in vivo, and drives reporter construct expression in vitro via two Htr2a promoter binding sites. These findings suggest that EGR3 directly regulates FC Htr2a expression in response to physiologic stimuli, providing a mechanism by which environment rapidly alters levels of a brain receptor that mediates symptoms, and treatment, of mental illness.One Sentence SummaryJust 6-8 hours of sleep deprivation upregulates brain levels of the receptor that mediates the response to hallucinogens.

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