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SAB1305978

Sigma-Aldrich

ANTI-IKB ALPHA (IKBA) antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Sinónimos:

IKBA, MAD3, NF-kappa-B inhibitor alpha, NFKBI, NFKBIA

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

35609 Da

species reactivity

human

technique(s)

western blot: 1:1000

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... NFKBIA(4792)

Physical form

Supplied in PBS with 0.09% (W/V) sodium azide

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

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

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Shirui Tan et al.
Molecular medicine reports, 19(3), 2057-2064 (2019-01-22)
The present study aimed to investigate the anti‑arthritic effects of curculigoside isolated from the rhizome of Curculigo orchioides Gaertn in vivo and in vitro, as well as to determine the potential underlying mechanisms. A rat model of arthritis was induced with type II
Caiguo Zhang et al.
Molecular oncology, 12(4), 476-494 (2018-01-30)
Cullin 4B, a member of the Cullins, which serve as scaffolds to facilitate the assembly of E3 ligase complexes, is aberrantly expressed in many cancers, including osteosarcoma. Recently, we observed that CUL4B forms the CRL4BDCAF11 E3 ligase, which specifically ubiquitinates
Yijia Wang et al.
Gut pathogens, 13(1), 2-2 (2021-01-14)
Inflammatory bowel disease caused by microbial dysbiosis is an important factor contributing to colorectal cancer (CRC) initiation. The 'driver-passenger' model in human gut microbial dysbiosis suggests that 'driver' bacteria may colonize with low relative abundance on tumor site but persistently

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