W1763 Colonic Expression of Claudin-2 Increases in Colitis and Colitis Associated Cancer (Cac) and is Regulated by EGF Receptor Activation in a Tissue Specific Manner

2010 ◽  
Vol 138 (5) ◽  
pp. S-735
Author(s):  
Rupesh Chaturvedi ◽  
Rizwan Ahmad ◽  
Mohammad Asim ◽  
Kay Washington ◽  
Keith T. Wilson ◽  
...  
Keyword(s):  
Egf Receptor ◽  
Receptor Activation ◽  
Tissue Specific ◽  
Specific Manner

Hypertension Increases Connexin43 in a Tissue-Specific Manner

Circulation ◽  
1997 ◽  
Vol 95 (4) ◽  
pp. 1007-1014 ◽  
Author(s):  
Jacques-Antoine Haefliger ◽  
Einar Castillo ◽  
Ge´rard Waeber ◽  
Gabriela E. Bergonzelli ◽  
Jean-Franc¸ois Aubert ◽  
...  
Keyword(s):  
Tissue Specific ◽  
Specific Manner

scholarly journals Tentacle Morphological Variation Coincides with Differential Expression of Toxins in Sea Anemones

Toxins ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 452
Author(s):  
Lauren M. Ashwood ◽  
Michela L. Mitchell ◽  
Bruno Madio ◽  
David A. Hurwood ◽  
Glenn F. King ◽  
...  
Keyword(s):  
Differential Expression ◽  
Morphological Variation ◽  
Expression Profiles ◽  
The Body ◽  
Sea Anemones ◽  
Tissue Specific ◽  
Venom Composition ◽  
Specific Manner ◽  
Branched Structures ◽  
Morphological Variants

Phylum Cnidaria is an ancient venomous group defined by the presence of cnidae, specialised organelles that serve as venom delivery systems. The distribution of cnidae across the body plan is linked to regionalisation of venom production, with tissue-specific venom composition observed in multiple actiniarian species. In this study, we assess whether morphological variants of tentacles are associated with distinct toxin expression profiles and investigate the functional significance of specialised tentacular structures. Using five sea anemone species, we analysed differential expression of toxin-like transcripts and found that expression levels differ significantly across tentacular structures when substantial morphological variation is present. Therefore, the differential expression of toxin genes is associated with morphological variation of tentacular structures in a tissue-specific manner. Furthermore, the unique toxin profile of spherical tentacular structures in families Aliciidae and Thalassianthidae indicate that vesicles and nematospheres may function to protect branched structures that host a large number of photosynthetic symbionts. Thus, hosting zooxanthellae may account for the tentacle-specific toxin expression profiles observed in the current study. Overall, specialised tentacular structures serve unique ecological roles and, in order to fulfil their functions, they possess distinct venom cocktails.

scholarly journals Syntaxin 1A Gene Is Negatively Regulated in a Cell/Tissue Specific Manner by YY1 Transcription Factor, Which Binds to the −183 to −137 Promoter Region Together with Gene Silencing Factors Including Histone Deacetylase

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 146
Author(s):  
Takahiro Nakayama ◽  
Toshiyuki Fukutomi ◽  
Yasuo Terao ◽  
Kimio Akagawa
Keyword(s):  
Transcription Factor ◽  
Gene Silencing ◽  
Protein Complex ◽  
Promoter Region ◽  
Neuronal Cell ◽  
Syntaxin 1A ◽  
Tissue Specific ◽  
Cell Tissue ◽  
Specific Manner ◽  
A Cell

The HPC-1/syntaxin 1A (Stx1a) gene, which is involved in synaptic transmission and neurodevelopmental disorders, is a TATA-less gene with several transcription start sites. It is activated by the binding of Sp1 and acetylated histone H3 to the −204 to +2 core promoter region (CPR) in neuronal cell/tissue. Furthermore, it is depressed by the association of class 1 histone deacetylases (HDACs) to Stx1a–CPR in non-neuronal cell/tissue. To further clarify the factors characterizing Stx1a gene silencing in non-neuronal cell/tissue not expressing Stx1a, we attempted to identify the promoter region forming DNA–protein complex only in non-neuronal cells. Electrophoresis mobility shift assays (EMSA) demonstrated that the −183 to −137 OL2 promoter region forms DNA–protein complex only in non-neuronal fetal rat skin keratinocyte (FRSK) cells which do not express Stx1a. Furthermore, the Yin-Yang 1 (YY1) transcription factor binds to the −183 to −137 promoter region of Stx1a in FRSK cells, as shown by competitive EMSA and supershift assay. Chromatin immunoprecipitation assay revealed that YY1 in vivo associates to Stx1a–CPR in cell/tissue not expressing Stx1a and that trichostatin A treatment in FRSK cells decreases the high-level association of YY1 to Stx1a-CPR in default. Reporter assay indicated that YY1 negatively regulates Stx1a transcription. Finally, mass spectrometry analysis showed that gene silencing factors, including HDAC1, associate onto the −183 to −137 promoter region together with YY1. The current study is the first to report that Stx1a transcription is negatively regulated in a cell/tissue-specific manner by YY1 transcription factor, which binds to the −183 to −137 promoter region together with gene silencing factors, including HDAC.

scholarly journals Retinoid nutritional status differently affects the expression of Japanese quail retinoic acid receptor-beta isoform transcripts in a tissue-specific manner

2001 ◽  
Vol 169 (2) ◽  
pp. 281-290 ◽  
Author(s):  
ZW Fu ◽  
T Kubo ◽  
K Sugahara ◽  
T Noguchi ◽  
H Kato
Keyword(s):  
Retinoic Acid ◽  
Nutritional Status ◽  
Japanese Quail ◽  
Retinoic Acid Receptor ◽  
Mrna Levels ◽  
Tissue Specific ◽  
Specific Manner ◽  
Lower Magnitude ◽  
Lung And Kidney ◽  
Receptor Beta

We investigated the effects of vitamin A (VA) nutritional status on the levels of expression of retinoic acid (RA) receptor-beta (RARbeta) gene in the various tissues of Japanese quail. VA deficiency caused a significant decrease in the mRNA levels of brain, liver, heart, lung and kidney RARbeta2/beta4, whereas no change was observed in the level of testis RARbeta2 transcript. In contrast, reduction in the RARbeta1 transcript caused by VA depletion was observed only in the lung, remaining unchanged in the other tissues. The administration of RA to the VA-deficient quail rapidly induced the expression of RARbeta2/beta4 mRNAs in all the tissues examined, but RA increased the expression of RARbeta1 transcript in the liver, heart, lung and kidney at a lower magnitude. RA could not change the expression of the brain RARbeta1 transcript, while it induced the expression of the testis RARbeta1 mRNA in a temporal way. These results clearly indicate that VA nutritional status differently regulates the expression of RARbeta1 and RARbeta2/beta4 transcripts in a tissue-specific manner.

The Sox-domain containing geneDichaete/fish-hookacts in concert withvndandindto regulate cell fate in theDrosophilaneuroectoderm

Development ◽  
2002 ◽  
Vol 129 (5) ◽  
pp. 1165-1174 ◽  
Author(s):  
Guoyan Zhao ◽  
James B. Skeath
Keyword(s):  
Cell Fate ◽  
Nerve Cord ◽  
Double Mutant ◽  
Ventral Nerve Cord ◽  
Egf Receptor ◽  
Dorsoventral Axis ◽  
Mutant Analysis ◽  
Evolutionarily Conserved ◽  
Specific Manner ◽  
Important Regulator

In the Drosophila embryonic central nervous system, neural stem cells, called neuroblasts, acquire fates in a position-specific manner. Recent work has identified a set of genes that functions along the dorsoventral axis to enable neuroblasts that develop in different dorsoventral domains to acquire distinct fates. These genes include the evolutionarily conserved transcription factors ventral nerve cord defective and intermediate neuroblasts defective, as well as the Drosophila EGF receptor. We show that the Sox-domain-containing gene Dichaete/fish-hook also plays a crucial role to pattern the neuroectoderm along the DV axis. Dichaete is expressed in the medial and intermediate columns of the neuroectoderm, and mutant analysis indicates that Dichaete regulates cell fate and neuroblast formation in these domains. Molecular epistasis tests, double mutant analysis and dosage-sensitive interactions demonstrate that during these processes, Dichaete functions in parallel with ventral nerve cord defective and intermediate neuroblasts defective, and downstream of EGF receptor signaling to mediate its effect on development. These results identify Dichaete as an important regulator of dorsoventral pattern in the neuroectoderm, and indicate that Dichaete acts in concert with ventral nerve cord defective and intermediate neuroblasts defective to regulate pattern and cell fate in the neuroectoderm.

scholarly journals EGF stimulates gastrin promoter through activation of Sp1 kinase activity

2000 ◽  
Vol 278 (4) ◽  
pp. C697-C708 ◽  
Author(s):  
Sergey Chupreta ◽  
Ming Du ◽  
Andrea Todisco ◽  
Juanita L. Merchant
Keyword(s):  
Kinase Activity ◽  
Egf Receptor ◽  
Solid Phase ◽  
Receptor Activation ◽  
Mitogen Activated Protein Kinase ◽  
Kinase Assay ◽  
Ags Cells ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

Epidermal growth factor (EGF) receptor activation stimulates gastrin gene expression through a GC-rich element called gastrin EGF response element (gERE). This element is bound by Sp1 family members and is a target of the ras-extracellular signal-regulated kinase (Erk) signal transduction cascade. This raised the possibility that Sp1 may be phosphorylated by kinases of this signaling pathway. Erk is capable of phosphorylating other mitogen-inducible transcription factors, e.g., Elk and Sap, suggesting that Erk may also mediate EGF-dependent phosphorylation of Sp1. This possibility was tested by studying Sp1-dependent kinase activity in extracts prepared from EGF-activated AGS cells by use of solid-phase kinase assays and immunoprecipitation of metabolically labeled Sp1. The results revealed that Sp1 kinase activity (like gastrin promoter activation) is inhibited by PD-98059 and, therefore, is dependent on mitogen-activated protein kinase kinase 1 (Mek 1). However, EGF-dependent activation of endogenous Erk did not account for most of the Sp1 kinase activity, since Erk and additional Sp1 kinase activity analyzed in a solid-phase kinase assay eluted from an ion-exchange column in different fractions. Phosphoamino acid analysis of in vivo radiolabeled Sp1 demonstrated that the kinase phosphorylates Sp1 on Ser and Thr in response to EGF. Therefore, most EGF-stimulated Sp1 kinase activity is Mek 1 dependent and distinct from Erk.

scholarly journals Targeting the EGF Receptor for Ovarian Cancer Therapy

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Reema Zeineldin ◽  
Carolyn Y. Muller ◽  
M. Sharon Stack ◽  
Laurie G. Hudson
Keyword(s):  
Ovarian Cancer ◽  
Targeted Therapies ◽  
Egf Receptor ◽  
Receptor Activation ◽  
Molecular Heterogeneity ◽  
Cancer Pathogenesis ◽  
The Us ◽  
The Status ◽  
Advanced Stages ◽  
Epidermal Growth

Ovarian carcinoma is the leading cause of death from gynecologic malignancy in the US. Factors such as the molecular heterogeneity of ovarian tumors and frequent diagnosis at advanced stages hamper effective disease treatment. There is growing emphasis on the identification and development of targeted therapies to disrupt molecular pathways in cancer. The epidermal growth factor (EGF) receptor is one such protein target with potential utility in the management of ovarian cancer. This paper will discuss contributions of EGF receptor activation to ovarian cancer pathogenesis and the status of EGF receptor inhibitors and EGF receptor targeted therapies in ovarian cancer treatment.

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