scholarly journals In Situ Chromatin-Binding Assay Using Epifluorescent Microscopy in S. pombe

2018 ◽  
pp. 155-165 ◽  
Author(s):  
Jinpu Yang ◽  
Fei Li
Keyword(s):  
Binding Assay ◽  
Chromatin Binding ◽  
Epifluorescent Microscopy

scholarly journals In Situ Binding Assay of Receptors for Vasoactive Peptides in Rat Aortic Rings by Quantitative Autoradiography

1993 ◽  
Vol 61 ◽  
pp. 257
Author(s):  
Haruyasu Ueda ◽  
Misato Takimoto ◽  
Yasushi Fujitani ◽  
Kyoko Oda ◽  
Toshikazu Okada ◽  
...  
Keyword(s):  
Binding Assay ◽  
Quantitative Autoradiography ◽  
Vasoactive Peptides

scholarly journals CITED1 is a novel binding partner of MITF that influences the MITF-directed transcriptional profile in melanoma

2017 ◽  
Author(s):  
Barbara Lettiero ◽  
Martin Lauss ◽  
Ake Borg ◽  
Sofia Gruvberger-Saal ◽  
Goran B Jönsson ◽  
...  
Keyword(s):  
Transcriptional Response ◽  
Gene Signature ◽  
Melanoma Cells ◽  
Cell Phenotype ◽  
Chromatin Binding ◽  
Binding Partner ◽  
Nuclear Complex ◽  
Number Of Genes ◽  
First Time

We previously demonstrated how CITED1 knockdown in melanoma cells had the capacity to perturb expression of a significant number of genes that comprised MITF and several of its known transcriptional targets. This manifest as a switch from a more invasive to a more proliferative gene signature phenotype. We now demonstrate by using MITF ChIP-seq, that altered CITED1 expression affects MITF transcription factor binding to its targets across the genome. We show that silencing CITED1 effectively amplifies the MITF chromatin-binding signal response while we also demonstrate for the first time that CITED1 and MITF co-localise in a nuclear complex using an in-situ ligation proximity assay. We propose that CITED1-MITF binding is capable of altering both the affinity of chromatin association and transcriptional response to MITF at the target regions in the genome where MITF is either directly or indirectly bound to DNA. As CITED1/SMAD2 has been shown to mediate TGFβ-driven transcription that induces amoeboid-like invasion in melanoma cells we hypothesis that the MITF/CITED1 driven transcriptional response dominates in MITF-high/low-invasive environment or proliferative signature cell phenotype, whereas the SMAD2/CITED1 transcriptional response is dominant in a low-MITF/ high-invasive signature environment.

scholarly journals CITED1 is a novel binding partner of MITF that influences the MITF-directed transcriptional profile in melanoma

2017 ◽  
Author(s):  
Barbara Lettiero ◽  
Martin Lauss ◽  
Ake Borg ◽  
Sofia Gruvberger-Saal ◽  
Goran B Jönsson ◽  
...  
Keyword(s):  
Transcriptional Response ◽  
Gene Signature ◽  
Melanoma Cells ◽  
Cell Phenotype ◽  
Chromatin Binding ◽  
Binding Partner ◽  
Nuclear Complex ◽  
Number Of Genes ◽  
First Time

We previously demonstrated how CITED1 knockdown in melanoma cells had the capacity to perturb expression of a significant number of genes that comprised MITF and several of its known transcriptional targets. This manifest as a switch from a more invasive to a more proliferative gene signature phenotype. We now demonstrate by using MITF ChIP-seq, that altered CITED1 expression affects MITF transcription factor binding to its targets across the genome. We show that silencing CITED1 effectively amplifies the MITF chromatin-binding signal response while we also demonstrate for the first time that CITED1 and MITF co-localise in a nuclear complex using an in-situ ligation proximity assay. We propose that CITED1-MITF binding is capable of altering both the affinity of chromatin association and transcriptional response to MITF at the target regions in the genome where MITF is either directly or indirectly bound to DNA. As CITED1/SMAD2 has been shown to mediate TGFβ-driven transcription that induces amoeboid-like invasion in melanoma cells we hypothesis that the MITF/CITED1 driven transcriptional response dominates in MITF-high/low-invasive environment or proliferative signature cell phenotype, whereas the SMAD2/CITED1 transcriptional response is dominant in a low-MITF/ high-invasive signature environment.

In situ fluorescence of lac dye stabilized gold nanoparticles; DNA binding assay and toxicity study

2016 ◽  
Vol 40 (8) ◽  
pp. 7121-7131 ◽  
Author(s):  
Sutanuka Pattanayak ◽  
Sharmila Chakraborty ◽  
Md. Masud Rahaman Mollick ◽  
Indranil Roy ◽  
Samita Basu ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Dna Binding ◽  
Binding Assay ◽  
Toxicity Study ◽  
Dna Interactions ◽  
Lac Dye ◽  
Dna Binding Assay

In situ synthesis of natural lac stabilized AuNPs, having DNA interactions and antitoxicity properties: UV-Vis and fluorimetric studies.

In Situ Binding Assay to Detect Myosin-1c Interactions with Hair-Cell Proteins

2007 ◽  
pp. 117-132
Author(s):  
Kelli R. Phillips ◽  
Janet L. Cyr
Keyword(s):  
Hair Cell ◽  
Binding Assay

scholarly journals Isolation of ras GTP-binding mutants using an in situ colony-binding assay.

1986 ◽  
Vol 83 (13) ◽  
pp. 4607-4611 ◽  
Author(s):  
L. A. Feig ◽  
B. T. Pan ◽  
T. M. Roberts ◽  
G. M. Cooper
Keyword(s):  
Binding Assay ◽  
Gtp Binding

scholarly journals Condensin II initiates sister chromatid resolution during S phase

2013 ◽  
Vol 200 (4) ◽  
pp. 429-441 ◽  
Author(s):  
Takao Ono ◽  
Daisuke Yamashita ◽  
Tatsuya Hirano
Keyword(s):  
Sister Chromatid ◽  
Chromosome Condensation ◽  
S Phase ◽  
Binding Property ◽  
Chromatin Binding ◽  
Structural Reorganization ◽  
Mitotic Entry ◽  
Replicative Stress ◽  
Chromosomal Loci

Condensins I and II are multisubunit complexes that play essential yet distinct functions in chromosome condensation and segregation in mitosis. Unlike condensin I, condensin II localizes to the nucleus during interphase, but it remains poorly understood what functions condensin II might have before mitotic entry. Here, we report that condensin II changes its chromatin-binding property during S phase. Remarkably, advanced premature chromosome condensation (PCC) assays enabled us to visualize condensin II forming “sister axes” in replicated regions of chromosomes in S phase cells. Depletion of condensin II compromised PCC-driven sister chromatid resolution during S phase. Moreover, fluorescence in situ hybridization assays revealed that condensin II, but not condensin I, promotes disjoining duplicated chromosomal loci during S phase. Application of mild replicative stress partially impaired this process and further exacerbated phenotypes arising from condensin II depletion. Our results suggest that condensin II initiates structural reorganization of duplicated chromosomes during S phase to prepare for their proper condensation and segregation in mitosis.

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