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Key Documents

PRS3967

Sigma-Aldrich

Anti-Cbl antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-Cas-BR-M murine ecotropic retro-viral transforming sequence, Anti-Cas-Br-M (murine) ecotropic retroviral transforming sequence, Anti-Casitas B-lineage lymphoma proto-oncogene

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About This Item

MDL number:
MFCD01633067
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

100

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

species reactivity

rat, mouse, human

technique(s)

indirect ELISA: suitable
indirect immunofluorescence: suitable
western blot: suitable

UniProt accession no.

P22681

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... CBL(867)

Related Categories

Immunogen

a 14 amino acid peptide from near the carboxy-terminus of human cbl.

Linkage

The action of this antibody can be blocked using blocking peptide SBP3967.

Physical form

Solution in phosphate buffered saline containing 0.02% sodium azide

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Product No.
Description
Pricing

Storage Class

10 - Combustible liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificates of Analysis (COA)

Lot/Batch Number
39670603
3967-0603

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Kristina Brand et al.
Human mutation, 35(11), 1372-1381 (2014-09-03)
Noonan syndrome, a congenital disorder comprising a characteristic face, short stature, heart defects, learning difficulties, and a predisposition to malignancies, is caused by heterozygous germline mutations in genes encoding components of RAS-MAPK signaling pathways. Mutations in the CBL tumor suppressor
Lasse Boding et al.
European journal of immunology, 44(10), 3109-3118 (2014-07-22)
Midline 1 (MID1) is a microtubule-associated ubiquitin ligase that regulates protein phosphatase 2A activity. Loss-of-function mutations in MID1 lead to the X-linked Opitz G/BBB syndrome characterized by defective midline development during embryogenesis. Here, we show that MID1 is strongly upregulated

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