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MAB5554

Sigma-Aldrich

Anti-Pax6 Antibody, clone AD1.5

ascites fluid, clone AD1.5, Chemicon®

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

100

antibody form

ascites fluid

antibody product type

primary antibodies

clone

AD1.5, monoclonal

species reactivity

zebrafish, rat, human, chicken, mouse

manufacturer/tradename

Chemicon®

technique(s)

immunohistochemistry: suitable
western blot: suitable

isotype

IgG1

NCBI accession no.

NM_000280.2
NM_001604.3

UniProt accession no.

P26367

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... PAX6(5080)

Specificity

Recognizes Pax6.

Immunogen

Recombinant human Pax6.

Application

Anti-Pax6 Antibody, clone AD1.5 is an antibody against Pax6 for use in IH & WB.
Research Category
Neuroscience
Research Sub Category
Developmental Neuroscience

Neuronal & Glial Markers
Western blot. The antibody recognizes the 46 and 48 kDa Pax6 proteins.Immunohistochemistry on frozen tissue sections.Optimal working dilutions must be determined by end user.

Target description

46 & 48 kDa

Physical form

Ascites fluid containing no preservatives.
Unpurified

Storage and Stability

Maintain for 1 year at -20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Analysis Note

Control
Embryonic eye tissue

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
This product can not be purchased for resale.

Legal Information

CHEMICON 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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Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

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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Gene, 534(2), 400-407 (2013-08-21)
In vitro neural differentiation of human embryonic stem cells (hESCs) is an advantageous system for studying early neural development. The process of early neural differentiation in hESCs begins by initiation of primitive neuroectoderm, which is manifested by rosette formation, with
Caroline A Johnson et al.
Development (Cambridge, England), 147(4) (2020-02-01)
Cellular and molecular mechanisms underlying the switch from self-amplification of cortical stem cells to neuronal and glial generation are incompletely understood, despite their importance for neural development. Here, we have investigated the role of the transcription factor specificity protein 2
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The fatal motor neuron (MN) disease Amyotrophic Lateral Sclerosis (ALS) is characterized by progressive MN degeneration. Phrenic MNs (phMNs) controlling the activity of the diaphragm are prone to degeneration in ALS, leading to death by respiratory failure. Understanding of the
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Molecular and cellular neurosciences, 109, 103562-103562 (2020-09-29)
Abnormal dendritic arbor development has been implicated in a number of neurodevelopmental disorders, such as autism and Rett syndrome, and the neuropsychiatric disorder schizophrenia. Postmortem brain samples from subjects with schizophrenia show elevated levels of NOS1AP in the dorsolateral prefrontal
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Cell reports, 32(4), 107962-107962 (2020-07-30)
Despite its clear impact on Alzheimer's disease (AD) risk, apolipoprotein (apo) E4's contributions to AD etiology remain poorly understood. Progress in answering this and other questions in AD research has been limited by an inability to model human-specific phenotypes in
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