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Flavonoids Redirect PIN-mediated Polar Auxin Fluxes during Root Gravitropic Responses
Santelia, D.,Henrichs, S.,Vincenzetti, V.,Sauer, M.,Bigler, L.,Klein, M.,Bailly, A.,Lee, Y.,Friml, J.,Geisler, M. The American Society for Biochemistry and Molecula 2008 The Journal of biological chemistry Vol.283 No.45
Identification of an ABCB/P-glycoprotein-specific Inhibitor of Auxin Transport by Chemical Genomics
Kim, J.-Y.,Henrichs, S.,Bailly, A.,Vincenzetti, V.,Sovero, V.,Mancuso, S.,Pollmann, S.,Kim, D.,Geisler, M.,Nam, H.-G. The American Society for Biochemistry and Molecula 2010 The Journal of biological chemistry Vol.285 No.30
Expression and Function of the ultraspiracle(usp) Gene during Development of Drosophila melanogaster
HAYDEN, MELISSA A.,HENRICH, VINCENT C.,BROWN, NEIL E.,SZEKELY, A. ALEX,LEPESANT, JEAN-ANTOINE,GILBERT, LAWRENCE I.,KIM, SE JAE,ANTONIEWSKI, CHRISTOPHE ANTONIEWSKI 濟州大學校 基礎科學硏究所 1995 基礎科學硏究 Vol.8 No.1
The usp locus encodes a member of the nuclear hormone receptor superfamily in Drosophila melanogaster that interacts with EcR(ecdysone receptor) to mediate ecdysteroid-induced gene expression. A 2.7-kb usp mRNA was detected at all developmental times tested, although its abundance varied. Among premetamorphic stages, both the 2.7-kb transcript and Usp protein attained their highest levels in the late third larval instar. The 2.7-kb usp transcript was also found in adult stages and a 1.2-kb transcript was detected in the polyadenylated RNA fraction of both mature adult females and early embryos. Aneuploids carrying two usp mutant alleles and a putative variegating ???? allele often developed deformities of the adult wing disc that apparently resulted from mutational disruption of usp activity before metamorphosis and whose frequency was affected by maternal genotype. Both of the recessive lethal usp mutations associated with this "cleft thorax" phenotype involved substitutions of conserved arginine residues in the DNA-binding domain, although the frequency of the phenotype was not the same for the two alleles. Both mutant proteins retained the ability to form heterodimers with EcR in vitro but showed reduced affinity for an ecdysone response element.
Acidic Fibroblast Growth Factor in Spinal Cord Injury
Chin-Chu Ko,Tsung-Hsi Tu,Jau-Ching Wu,Wen-Cheng Huang,Henrich Cheng 대한척추신경외과학회 2019 Neurospine Vol.16 No.4
Spinal cord injury (SCI), with an incidence rate of 246 per million person-years among adults in Taiwan, remains a devastating disease in the modern day. Elderly men with lower socioeconomic status have an even higher risk for SCI. Despite advances made in medicine and technology to date, there are few effective treatments for SCI due to limitations in the regenerative capacity of the adult central nervous system. Experiments and clinical trials have explored neuro-regeneration in human SCI, encompassing cell- and molecule-based therapies. Furthermore, strategies have aimed at restoring connections, including autologous peripheral nerve grafts and biomaterial scaffolds that theoretically promote axonal growth. Most molecule-based therapies target the modulation of inhibitory molecules to promote axonal growth, degrade glial scarring obstacles, and stimulate intrinsic regenerative capacity. Among them, acidic fibroblast growth factor (aFGF) has been investigated for nerve repair; it is mitogenic and pluripotent in nature and could enhance axonal growth and mitigate glial scarring. For more than 2 decades, the authors have conducted multiple trials, including human and animal experiments, using aFGF to repair nerve injuries, including central and peripheral nerves. In these trials, aFGF has shown promise for neural regeneration, and in the future, more trials and applications should investigate aFGF as a neurotrophic factor. Focusing on aFGF, the current review aimed to summarize the historical evolution of the utilization of aFGF in SCI and nerve injuries, to present applications and trials, to summarize briefly its possible mechanisms, and to provide future perspectives.
Al Ghouleh, Imad,Meijles, Daniel N.,Mutchler, Stephanie,Zhang, Qiangmin,Sahoo, Sanghamitra,Gorelova, Anastasia,Henrich Amaral, Jefferson,Rodré,í,guez, André,s I.,Mamonova, Tatyana,So National Academy of Sciences 2016 Proceedings of the National Academy of Sciences Vol.113 No.36
<P>Despite numerous reports implicating NADPH oxidases (Nox) in the pathogenesis of many diseases, precise regulation of this family of professional reactive oxygen species (ROS) producers remains unclear. A unique member of this family, Nox1 oxidase, functions as either a canonical or hybrid system using Nox organizing subunit 1 (NoxO1) or p47(phox), respectively, the latter of which is functional in vascular smooth muscle cells (VSMC). In this manuscript, we identify critical requirement of ezrin-radixin-moesin-binding phosphoprotein 50 (EBP50; aka NHERF1) for Nox1 activation and downstream responses. Superoxide (O-2(center dot-)) production induced by angiotensin II (AngII) was absent in mouse EBP50 KO VSMC vs. WT. Moreover, ex vivo incubation of aortas with AngII showed a significant increase in O-2(center dot-)-in WT but not EBP50 or Nox1 nulls. Similarly, lipopolysaccharide (LPS)-induced oxidative stress was attenuated in femoral arteries from EBP50 KO vs. WT. In silico analyses confirmed by confocal microscopy, immunoprecipitation, proximity ligation assay, FRET, and gain-/ loss-of-function mutagenesis revealed binding of EBP50, via its PDZ domains, to a specific motif in p47(phox). Functional studies revealed AngII-induced hypertrophy was absent in EBP50 KOs, and in VSMC overexpressing EBP50, Nox1 gene silencing abolished VSMC hypertrophy. Finally, ex vivo measurement of lumen diameter in mouse resistance arteries exhibited attenuated AngII-induced vasoconstriction in EBP50 KO vs. WT. Taken together, our data identify EBP50 as a previously unidentified regulator of Nox1 and support that it promotes Nox1 activity by binding p47(phox). This interaction is pivotal for agonist-induced smooth muscle ROS, hypertrophy, and vasoconstriction and has implications for ROS-mediated physiological and pathophysiological processes.</P>