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MAB390-100UG

Sigma-Aldrich

Anti-p75 LNGFR Antibody, Saporin conjugated, clone 192

clone 192, Chemicon®, from mouse

Synonym(s):

p75 Low Affinity Neurotrophin Receptor, NGFR

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About This Item

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

biological source

mouse

Quality Level

conjugate

saporin

antibody product type

primary antibodies

clone

192, monoclonal

species reactivity

rat

should not react with

mouse, human

manufacturer/tradename

Chemicon®

technique(s)

immunolesioning: suitable

isotype

IgG1

NCBI accession no.

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... NGFR(4804)

Specificity

Rat NGF receptor. MAB365 is the monoclonal antibody used for MAB390-SAP

Application

Anti-p75 Low Affinity Nerve Growth Factor Receptor Antibody, Saporin conjugated, clone 192 is an antibody against p75 Low Affinity Nerve Growth Factor Receptor for use in 0.
Immunotoxin (see "Protocols" for Technical Notes)
Research Category
Neuroscience
Research Sub Category
Neurodegenerative Diseases

Neurochemistry & Neurotrophins

Physical form

Saporin Conjugated. 192-IgG-SAP is sterile filtered and presented in Dulbecco′s PBS with no preservative.

Storage and Stability

Centrifuge material at low speed in microfuge to ensure all of the solution is at the bottom of the tube. Vortex gently. Long term storage at -70ºC or below. Short term storage at -20ºC or 2-8ºC with appropriate antibacterial agent if compatible with the intended application. The sterile conjugate is stable at 2-8ºC for several months. Avoid repeated freezing and thawing. Glycerol (1:1) can be added for additional stability if compatible with the intended application. This immunotoxin may be handled safely using standard laboratory procedures as the cross-species reactivity between these anti-rat p75 antibodies and the human form of p75 is negligible.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

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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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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Removal of cholinergic input to rat posterior parietal cortex disrupts incremental processing of conditioned stimuli.
Bucci, D J, et al.
The Journal of Neuroscience, 18, 8038-8046 (1998)
Basal forebrain cholinergic lesions disrupt increments but not decrements in conditioned stimulus processing.
Chiba, A A, et al.
The Journal of Neuroscience, 15, 7315-7322 (1995)
J J Waite et al.
Neuroscience, 65(2), 463-476 (1995-03-01)
Immunolesions of the cholinergic basal forebrain were produced in rats using various intraventricular doses of the immunotoxin 192 immunoglobulin G-saporin: 0.34, 1.34, 2.0, 2.7 and 4.0 micrograms/rat. A battery of behavioral tests, chosen on the basis of reported sensitivity to
J Apelt et al.
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 15(1), 95-112 (1997-02-01)
Pathological processing of the amyloid precursor protein (APP) is assumed to be responsible for the amyloid deposits in Alzheimer-diseased brain tissue, but the physiological function of this protein in the brain is still unclear. The aim of this study is
Coadministration of galanin antagonist M40 with a muscarinic M1 agonist improves delayed nonmatching to position choice accuracy in rats with cholinergic lesions.
McDonald, M P, et al.
The Journal of Neuroscience, 18, 5078-5085 (1998)

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