scholarly journals Prolonged Fasting Increases Nrf2 Nuclear Accumulation and DNA Binding Ability in Postweaned Northern Elephant Seals

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Jose Pablo Vazquez-Medina ◽  
Jose Guadalupe Soñanez-Organis ◽  
Jose Abraham Viscarra ◽  
Michael S Tift ◽  
Henry Jay Forman ◽  
...  
2012 ◽  
Vol 215 (9) ◽  
pp. 1448-1455 ◽  
Author(s):  
J. G. Sonanez-Organis ◽  
J. P. Vazquez-Medina ◽  
T. Zenteno-Savin ◽  
A. Aguilar ◽  
D. E. Crocker ◽  
...  

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Jose Pablo Vazquez‐Medina ◽  
Cory Champagne ◽  
C Leo Ortiz ◽  
Daniel E Crocker ◽  
Rudy M Ortiz

2011 ◽  
Vol 214 (8) ◽  
pp. 1294-1299 ◽  
Author(s):  
J. P. Vazquez-Medina ◽  
T. Zenteno-Savin ◽  
H. J. Forman ◽  
D. E. Crocker ◽  
R. M. Ortiz

2012 ◽  
Author(s):  
Colleen Reichmuth ◽  
Caroline Casey ◽  
Isabelle Charrier ◽  
Nicolas Mathevon ◽  
Brandon Southall

1994 ◽  
Vol 14 (11) ◽  
pp. 7557-7568 ◽  
Author(s):  
J Zuo ◽  
R Baler ◽  
G Dahl ◽  
R Voellmy

Heat stress regulation of human heat shock genes is mediated by human heat shock transcription factor hHSF1, which contains three 4-3 hydrophobic repeats (LZ1 to LZ3). In unstressed human cells (37 degrees C), hHSF1 appears to be in an inactive, monomeric state that may be maintained through intramolecular interactions stabilized by transient interaction with hsp70. Heat stress (39 to 42 degrees C) disrupts these interactions, and hHSF1 homotrimerizes and acquires heat shock element DNA-binding ability. hHSF1 expressed in Xenopus oocytes also assumes a monomeric, non-DNA-binding state and is converted to a trimeric, DNA-binding form upon exposure of the oocytes to heat shock (35 to 37 degrees C in this organism). Because endogenous HSF DNA-binding activity is low and anti-hHSF1 antibody does not recognize Xenopus HSF, we employed this system for mapping regions in hHSF1 that are required for the maintenance of the monomeric state. The results of mutagenesis analyses strongly suggest that the inactive hHSF1 monomer is stabilized by hydrophobic interactions involving all three leucine zippers which may form a triple-stranded coiled coil. Trimerization may enable the DNA-binding function of hHSF1 by facilitating cooperative binding of monomeric DNA-binding domains to the heat shock element motif. This view is supported by observations that several different LexA DNA-binding domain-hHSF1 chimeras bind to a LexA-binding site in a heat-regulated fashion, that single amino acid replacements disrupting the integrity of hydrophobic repeats render these chimeras constitutively trimeric and DNA binding, and that LexA itself binds stably to DNA only as a dimer but not as a monomer in our assays.


1991 ◽  
Vol 5 (10) ◽  
pp. 1902-1911 ◽  
Author(s):  
K D Sarge ◽  
V Zimarino ◽  
K Holm ◽  
C Wu ◽  
R I Morimoto

Author(s):  
Mina Hanifeh Ahagh ◽  
Gholamreza Dehghan ◽  
Majid Mahdavi ◽  
Mohammad Ali Hosseinpour Feizi ◽  
Reza Teimuri-Mofrad ◽  
...  

2021 ◽  
Author(s):  
Chaofan Peng ◽  
Yuqian Tan ◽  
Peng Yang ◽  
Kangpeng Jin ◽  
Chuan Zhang ◽  
...  

Abstract BackgroundEmerging studies have investigated circRNAs as significant regulation factors in multiple cancer progression. Nevertheless, the biological functions and underlying mechanisms of circRNAs in colorectal cancer progression remain unclear.MethodsA novel circRNA (circ-GALNT16) was identified by microarray and qRT-PCR. A series of phenotype experiments in vitro and vivo were performed to investigate the role of circ-GALNT16 in CRC. FISH, RNA pulldown assay, RIP assay, RNA sequencing, coimmunoprecipitation, and ChIP were constructed to explore the molecular mechanisms of circ-GALNT16 in colorectal cancer.ResultsCirc-GALNT16 was downregulated in colorectal cancer and negatively correlated with poor prognosis. Circ-GALNT16 suppressed the proliferation and metastasis ability of colorectal cancer in vitro and vivo. Mechanistically, circ-GALNT16 could bind to the KH3 domain of heterogeneous nuclear ribonucleoprotein K (hnRNPK), which resulted in the SUMOylation of hnRNPK. Additionally, circ-GALNT16 could enhance the hnRNPK-p53 complex by facilitating the SUMOylation of hnRNPK. Furthermore, RNA sequencing assay identified serpin family E member 1 as the target gene of circ-GALNT16 at the transcriptional level. Rescue assays revealed that circ-GALNT16 regulated the expression of Serpine1 by inhibiting the deSUMOylation of hnRNPK mediated by SUMO specific peptidase 2 and then regulating the sequence-specific DNA binding ability of the hnRNPK-p53 transcriptional complex.ConclusionsCirc-GALNT16 suppressed CRC progression via inhibiting Serpine1 expression through adjusting the sequence-specific DNA binding ability of the SENP2-mediated hnRNPK-p53 transcriptional complex and might work as a biomarker and therapeutic target for CRC.


2018 ◽  
Vol 285 (1892) ◽  
pp. 20182176 ◽  
Author(s):  
Caroline Casey ◽  
Colleen Reichmuth ◽  
Daniel P. Costa ◽  
Burney Le Boeuf

Vocal dialects are fundamental to our understanding of the transmission of social behaviours between individuals and populations, however few accounts trace this phenomenon among mammals over time. Northern elephant seals ( Mirounga angustirostris ) provide a rare opportunity to examine the trajectory of dialects in a long-lived mammalian species. Dialects were first documented in the temporal patterns of the stereotyped vocal displays produced by breeding males at four sites in the North Pacific in 1968 and 1969, as the population recovered from extreme exploitation. We evaluated the longevity of these geographical differences by comparing these early recordings to calls recently recorded at these same locations. While the presence of vocal dialects in the original recordings was re-confirmed, geographical differences in vocal behaviour were not found at these breeding rookeries nearly 50 years later. Moreover, the calls of contemporary males displayed more structural complexity after approximately four generations, with substantial between-individual variation and call features not present in the historical data. In the absence of measurable genetic variation in this species—owing to an extreme population bottleneck—a combination of migration patterns and cultural mutation are proposed as factors influencing the fall of dialects and the dramatic increase in call diversity.


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