A signal-on photoelectrochemical biosensor for detecting cancer marker type IV collagenase by coupling enzyme cleavage with exciton energy transfer biosensing

2019 ◽  
Vol 11 (46) ◽  
pp. 5880-5885 ◽  
Author(s):  
Jiexia Chen ◽  
Guang-Chao Zhao ◽  
Yan Wei ◽  
Dexiang Feng
Keyword(s):  
Energy Transfer ◽  
Exciton Energy ◽  
Ag Nps ◽  
Type Iv Collagenase ◽  
Cancer Marker ◽  
Type Iv ◽  
Marker Type ◽  
Enzyme Cleavage ◽  
Photoelectrochemical Biosensor ◽  
Hydrolysis Of

A signal-on photoelectrochemical biosensor was developed for the sensitive detection of a cancer marker type IV collagenase, which relied on the exciton energy transfer between CdTe QDs and Ag NPs combined with the catalytic hydrolysis of protease.

A sensitive and selective quantum dots-based FRET biosensor for the detection of cancer marker type IV collagenase

2011 ◽  
Vol 3 (8) ◽  
pp. 1797 ◽  
Author(s):  
Hongying Liu ◽  
Guoxi Liang ◽  
E. S. Abdel-Halim ◽  
Jun-Jie Zhu
Keyword(s):  
Quantum Dots ◽  
Type Iv Collagenase ◽  
Cancer Marker ◽  
Type Iv ◽  
Marker Type

Induction of tissue-type plasminogen activator and 72-kDa type-IV collagenase by ionizing radiation in rat astrocytes

1994 ◽  
Vol 56 (2) ◽  
pp. 214-218 ◽  
Author(s):  
Raymond Sawaya ◽  
Philip J. Tofion ◽  
Sanjeeva Mohanam ◽  
Francis Ali-Oosman ◽  
Lance A. Liotta ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Plasminogen Activator ◽  
Tissue Type ◽  
Type Iv Collagenase ◽  
Tissue Type Plasminogen Activator ◽  
Type Iv ◽  
Type Plasminogen Activator ◽  
Rat Astrocytes

Positive and negative transcriptional elements of the human type IV collagenase gene

1990 ◽  
Vol 10 (12) ◽  
pp. 6524-6532
Author(s):  
S M Frisch ◽  
J H Morisaki
Keyword(s):  
Core Promoter ◽  
Type Iv Collagenase ◽  
Mobility Shift ◽  
Specific Expression ◽  
Enhancer Element ◽  
Type Iv ◽  
Dnase I Footprinting ◽  
Gel Mobility Shift ◽  
Transcriptional Elements ◽  
Mcf 7

Proteolysis by type IV collagenase (T4) has been implicated in the process of tumor metastasis. The T4 gene is expressed in fibroblasts, but not in normal epithelial cells, and its expression is specifically repressed by the E1A oncogene of adenovirus. We present an investigation of the transcriptional elements responsible for basal, E1A-repressible, and tissue-specific expression. 5'-Deletion analysis, DNase I footprinting, and gel mobility shift assays revealed a strong, E1A-repressible enhancer element, r2, located about 1,650 bp upstream of the start site. This enhancer bound a protein with binding specificity very similar to that of the transcription factor AP-2. A potent silencer sequence was found 2 to 5 bp downstream of this enhancer. The silencer repressed transcription from either r2 or AP-1 enhancer elements and in the context of either type IV collagenase or thymidine kinase (tk) gene core promoters; enhancerless transcription from the latter core promoter was also repressed. Comprising the silencer were two contiguous, autonomously functioning silencer elements. Negative regulation of T4 transcription by at least two factors was demonstrated. mcf-7 proteins specifically binding both elements were detected by gel mobility shift assays; a protein of approximately 185 kDa that bound to one of these elements was detected by DNA-protein cross-linking. The silencer repressed transcription, in an r2 enhancer-tk promoter context, much more efficiently in T4-nonproducing cells (mcf-7 or HeLa) than in T4-producing cells (HT1080), suggesting that cell type-specific silencing may contribute to the regulation of this gene.

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