Thermo Fisher Scientific IkB alpha Monoclonal Antibody (MFRDTRK), APC, eBioscience
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카탈로그 번호 | CAS 번호 | 설명 | 상태 | 단위 | 판매가 | 할인가 | 가격(VAT포함) | 수량 / 장바구니 / 찜 |
17-9036-42 | - | Thermo Fisher Scientific 17-9036-42 IkB alpha Monoclonal Antibody (MFRDTRK), APC, eBioscience 100 tests pk | 재고문의 | pk | 635,000원 | - | 698,500원 |
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Applications
Tested Dilution
Publications
Flow Cytometry (Flow)
5 µL (0.125 µg)/test
Product Specifications
Species Reactivity
Human, Mouse
Host/Isotype
Rat / IgG2b, kappa
Recommended Isotype Control
Rat IgG2b kappa Isotype Control (eB149/10H5), APC, eBioscience™
Class
Monoclonal
Type
Antibody
Clone
MFRDTRK
Conjugate
APC APC APC
View additional formats
Excitation/Emission Max
651/660 nm View spectra
Form
Liquid
Concentration
5 µL/Test
Purification
Affinity chromatography
Storage buffer
PBS, pH 7.2, with 0.2% BSA
Contains
0.09% sodium azide
Storage conditions
4° C, store in dark, DO NOT FREEZE!
Shipping conditions
Ambient (domestic); Wet ice (international)
RRID
AB_2762604
Product Specific Information
Description: This MFRDTRK monoclonal antibody recognizes human and mouse nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha (I kappa B alpha). I kappa B alpha is one member of a family of cellular proteins that functions to inhibit classical/canonical NF-kappa B signaling by masking the nuclear localization signals (NLS) of NF-kappa B proteins and keeping them sequestered in an inactive state in the cytoplasm. Classical/canonical NF-kappa B signaling is initiated in response to myriad stimuli including engagement of T cell and B cell receptors, growth factors, and inflammatory stimuli (reactive oxygen species, TNF alpha, IL-1) and results in the activation of the I kappa B kinase (IKK) complex that includes IKK alpha, IKK beta, and NEMO. IKK phosphorylates I kappa B alpha resulting in its ubiquitination, degradation, and subsequent translocation of NF-kappa B transcription factor proteins into the nucleus.
Applications Reported: This MFRDTRK antibody has been reported for use in flow cytometric analysis.
Applications Tested: This MFRDTRK antibody has been pre-diluted and tested by flow cytometric analysis of normal human peripheral blood cells. This may be used at 5 µL (0.125 µg) per test. A test is defined as the amount (µg) of antibody that will stain a cell sample in a final volume of 100 µL. Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test.
Excitation: 633-647 nm; Emission: 660 nm; Laser: Red Laser
Target Information
IkB-alpha is a 40 kDa protein that functions to inhibit NF- kappaB activity. The inhibition occurs via protein-protein interaction between I kappaB proteins and NF- kappaB dimers in the cytosol. The interaction of I kappa B-alpha with NF- kappaB masks the nuclear localization sequence of NF- kappaB, preventing NF- kappaB translocation to the nucleus. A variety of stimuli can activate gene expression by liberating NF- kappaB through the degradation of I kappaB alpha. These stimuli include the proinflammatory cytokines TNF- alpha and IL-1 beta, chemokines, PMA, growth factors, LPS, UV irradiation, viral infection, as well as various chemical and physical stresses. In humans, the gene is located on the q arm of chromosome 14. Activation of NFkB requires that IkB be phosphorylated on specific serine residues, which results in targeted degradation of IkB. IkB kinase alpha (IKK alpha), previously designated CHUK, interacts with IkB-alpha and specifically phosphorylates IkB-alpha on the sites that trigger its degradation Serines 32 and 36. IKK alpha appears to be critical for NFkB activation in response to proinflammatory cytokines. Phosphorylation of IkB by IKK alpha is stimulated by the NFkB inducing kinase (NIK), which itself is a central regulator for NFkB activation in response to TNF and IL-1. The functional IKK complex contains three subunits, IKK alpha, IKK beta and IKK gamma, and each appear to make essential contributions to IkB phosphorylation.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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