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Sigma-Aldrich

Nunc® MicroWell® MiniTrays

60 well MicroWell MiniTray for serological applications, non-treated, polystyrene, non-sterile, 100/cs

Synonym(s):

micro well plate, microwell plates, mini trays

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About This Item

UNSPSC Code:
41122107
NACRES:
NB.22

material

flat bottom clear polystyrene wells
polystyrene

sterility

non-sterile

feature

lid
lid
low profile

packaging

case of 100 (internal packs of 10)

manufacturer/tradename

Nunc 439225

external L × W

84 mm × 59 mm , w/ lid

maximum volume

10 μL

size

60 wells

surface area

0.2 cm2 , total surface area (cm2)

well maximum volume

10 μm

working volume

10 μL

color

clear

suitability

suitable for (serological applications)
suitable for (serotyping, microcytotoxicity and cell cloning studies)

binding type

non-treated surface

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General description


  • Used in serotyping, microcytotoxicity and cell cloning studies
  • Optical clarity allows use with inverted microscopes
  • Occupy minimal freezer and incubator space
  • Lids have keyed tabs for proper orientation
  • Large raised alpha-numeric coordinates
  • Unique surface treatment to enhance sample and reagent mixing

Legal Information

MicroWell is a trademark of Thermo Fisher Scientific or its subsidiaries
Nunc is a registered trademark of Thermo Fisher Scientific or its subsidiaries

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Mariana C C Silva et al.
The Journal of cell biology, 219(4) (2020-04-25)
Cohesin is essential for genome folding and inheritance. In somatic cells, these functions are both mediated by Scc1-cohesin, which in mitosis is released from chromosomes by Wapl and separase. In mammalian oocytes, cohesion is mediated by Rec8-cohesin. Scc1 is expressed
Iris Schäffner et al.
Neuron, 99(6), 1188-1203 (2018-09-11)
Autophagy is a conserved catabolic pathway with emerging functions in mammalian neurodevelopment and human neurodevelopmental diseases. The mechanisms controlling autophagy in neuronal development are not fully understood. Here, we found that conditional deletion of the Forkhead Box O transcription factors FoxO1

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