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Key Documents

MAB5488

Sigma-Aldrich

Anti-CRABP2 Antibody

ascites fluid, Chemicon®

Synonym(s):

CRABPII

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About This Item

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

biological source

mouse

Quality Level

antibody form

ascites fluid

antibody product type

primary antibodies

clone

monoclonal

species reactivity

mouse, human

manufacturer/tradename

Chemicon®

technique(s)

ELISA: suitable
immunocytochemistry: suitable
western blot: suitable

isotype

IgG2a

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... CRABP2(1382)

Specificity

Reacts with Cellular Retinoic Acid Binding Protein II (CRABPII). No cross reactivity with CRABPI.

Immunogen

Full length recombinant human CRABPII.

Application

Use Anti-CRABP2 Antibody (Mouse Monoclonal Antibody) validated in ELISA, WB, ICC to detect CRABP2 also known as Cellular Retinoic Acid Binding Protein II.

Legal Information

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

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Storage Class Code

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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T cell anergy is one of the mechanisms contributing to peripheral tolerance, particularly in the context of progressively growing tumors and in tolerogenic treatments promoting allograft acceptance. We recently reported that early growth response gene 2 (Egr2) is a critical
Shuiliang Yu et al.
Journal of experimental & clinical cancer research : CR, 41(1), 88-88 (2022-03-10)
Resistance to standard therapy is a major reason for the poor prognosis of pancreatic ductal adenocarcinoma (PDAC). Developing novel therapy to overcome PDAC drug-resistance is urgently needed. CRABP-II was highly expressed in all PDAC but not expressed in normal pancreatic
Matt J Matrongolo et al.
Development (Cambridge, England), 150(18) (2023-08-17)
Secondary lissencephaly evolved in mice due to effects on neurogenesis and the tangential distribution of neurons. Signaling pathways that help maintain lissencephaly are still poorly understood. We show that inactivating Twist1 in the primitive meninges causes cortical folding in mice.

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