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Merck
CN

438192

Anti-LRP, Light Chain Mouse mAb (5A6)

liquid, clone 5A6, Calbiochem®

Synonym(s):

Anti-Low Density Lipoprotein Receptor-Related Protein

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About This Item

NACRES:
NA.43
UNSPSC Code:
12352203

Key Documents

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Product Name

Anti-LRP, Light Chain Mouse mAb (5A6), liquid, clone 5A6, Calbiochem®

biological source

mouse

antibody form

purified antibody

antibody product type

primary antibodies

clone

5A6, monoclonal

form

liquid

does not contain

preservative

species reactivity

rabbit, mouse, human

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
avoid repeated freeze/thaw cycles

dilution

(Frozen Sections (1-5 µg/mL)
Immunoblotting (1-5 µg/mL)
Paraffin Sections (1-5 µg/mL, )

isotype

IgG2

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

100

Gene Information

human ... LRP1(4035)

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Preparation Note

Following initial thaw, aliquot and freeze (-20°C).

Application

Frozen Sections (1-5 µg/ml)

Immunoblotting (1-5 µg/ml)

Paraffin Sections (1-5 µg/ml, see application references)

Disclaimer

Toxicity: Standard Handling (A)

General description

Purified mouse monoclonal antibody. Recognizes the ~85 kDa LRP light chain protein under non-reducing conditions.
Recognizes the ~85 kDa LRP protein.
This Anti-LRP, Light Chain Mouse mAb (5A6) is validated for use in Frozen Sections, Immunoblotting, Paraffin Sections for the detection of LRP, Light Chain.

Immunogen

Human
purified, human placenta LRP

Other Notes

Mikhailenko, I., et al. 2001. J. Biol. Chem.276, 39484.
Rebeck, W.G., et al. 2001. Mol. Brain Res.87, 238.
Coukos, G., et al. 1994. Am. J. Pathol.144, 383.
Daugherty, A., and Rateri, D.L. 1994. Arterioscler Thromb.14, 2017.
Strickland, D.K., et al. 1990. J. Biol. Chem.265, 17401.
Variables associated with assay conditions will dictate the proper working dilution.

Packaging

Please refer to vial label for lot-specific concentration.

Physical form

In 100 mM NaCl, 50 mM sodium phosphate, 1 mM EDTA, pH 6.6.

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Storage Class

10 - Combustible liquids

wgk

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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Robert D Bell et al.
Nature cell biology, 11(2), 143-153 (2008-12-23)
Amyloid beta-peptide (Abeta) deposition in cerebral vessels contributes to cerebral amyloid angiopathy (CAA) in Alzheimer's disease (AD). Here, we report that in AD patients and two mouse models of AD, overexpression of serum response factor (SRF) and myocardin (MYOCD) in
Junling Yang et al.
Journal of molecular neuroscience : MN, 49(2), 277-288 (2012-09-05)
We previously reported that anti-amyloid-beta (Aβ) single-chain antibody (scFv59) brain delivery via recombinant adeno-associated virus (rAAV) was effective in reducing cerebral Aβ load in an Alzheimer's disease (AD) mouse model without inducing inflammation. Here, we investigated the prophylactic effects and
Abhay P Sagare et al.
The Journal of biological chemistry, 288(21), 15154-15166 (2013-04-13)
Soluble low density lipoprotein receptor-related protein-1 (sLRP1) binds ~70% of amyloid β-peptide (Aβ) in human plasma. In Alzheimer disease (AD) and individuals with mild cognitive impairment converting to AD, plasma sLRP1 levels are reduced and sLRP1 is oxidized, which results
Arne Herring et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 26(1), 117-128 (2011-09-29)
Physical activity protects brain function in healthy individuals and those with Alzheimer's disease (AD). Evidence for beneficial effects of parental exercise on the health status of their progeny is sparse and limited to nondiseased individuals. Here, we questioned whether maternal
Tomomi Kiyota et al.
Journal of neuroimmunology, 319, 80-92 (2018-03-27)
We investigated the effects of granulocyte-macrophage colony stimulating factor (GM-CSF) on behavioral and pathological outcomes in Alzheimer's disease (AD) and non-transgenic mice. GM-CSF treatment in AD mice reduced brain amyloidosis, increased plasma Aβ, and rescued cognitive impairment with increased hippocampal
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