WBAVDFL01
Immobilon® Block - FL (Fluorescent Blocker)
Fluorescent Detection for Western blotting, dot/slot blotting, mass spectrometry and fluorescence assays
Synonym(s):
Fluorescent Blocker, Immobilon Blocking Reagent
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About This Item
UNSPSC Code:
41116010
eCl@ss:
42029053
NACRES:
NB.22
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Quality Level
packaging
pkg of 500 mL
manufacturer/tradename
Immobilon®
technique(s)
western blot: suitable
membrane area
1000 cm2 , membrane coverage
detection method
fluorometric
shipped in
ambient
storage temp.
15-25°C
General description
Immobilon® Block Noise Cancelling Reagents are designed especially for Western blotting applications. This family of protein-free, ready-to-use buffers has been optimized to reduce background levels when using chemiluminescence, fluorescent, or phosphotyrosine detection. Bløk buffers are ideal for use with Immobilon-P Western blotting membranes and the SNAP i.d. system, and are also compatible with standard Western blotting techniques.
Application
For use on immunoblots.
Packaging
Sufficient reagent for 19 mini blots (8x7 cm)
Quality
For optimum results, use Immobilon-P membrane for chemiluminescence (luminol) or visual detection (e.g. TMB), and Immobilon-FL membrane for fluorescent detection applications.
Storage and Stability
Stable for 2 years at 20–25°C
Legal Information
Immobilon is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Warning
hcodes
flash_point_f
does not flash
flash_point_c
does not flash
Certificates of Analysis (COA)
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Yann Ehinger et al.
EMBO molecular medicine, 12(2), e10889-e10889 (2020-01-09)
Mutations in the X-linked MECP2 gene are responsible for Rett syndrome (RTT), a severe neurological disorder for which there is no treatment. Several studies have linked the loss of MeCP2 function to alterations of brain-derived neurotrophic factor (BDNF) levels, but
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