antibody

Rabbit anti IkBa Polyclonal antibody

MBS462221

0.1 mg

250 USD

polyclonal

rabbit

nonconjugated

human, mouse, rat, dog, chicken, cow

western blot, ELISA, immunohistochemistry

Antibody

Rabbit anti IkBa Polyclonal antibody

IkBa (NFKB1A)

Rabbit anti-IkBa; I kappa B alpha; IkBa; IkappaBalpha; MAD3.

IkBa; NF-kappa-B inhibitor alpha; NF-kappa-B inhibitor alpha; ikB-alpha; IkappaBalpha; I-kappa-B-alpha; OTTHUMP00000178842; nuclear factor of kappa light chain gene enhancer in B-cells; major histocompatibility complex enhancer-binding protein MAD3; nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha; I-kappa-B-alpha; IkB-alpha; IkappaBalpha; Major histocompatibility complex enhancer-binding protein MAD3

IkBa (NFKB1A)

NFKBIA; NFKBIA; IKBA; MAD-3; NFKBI; IKBA; MAD3; NFKBI

IKBA_HUMAN

Polyclonal

Rabbit

Human, Rat, Mouse, Bovine, Chicken, Dog

This antibody recognizes ~42 kDa of human IkBa. This antibody also reacts with rat and mouse. The other species are not tested.

The Rabbit IgG is purified by Site-specific Epitope Affinity Purification.

This affinity purified antibody is supplied in sterile Phosphatebuffered saline (pH7.2) containing antibody stabilizer

Size: 100 ug/200 ul

The antibodies are stable for 12 months from date of receipt when stored at -20 degree C to -70 degree C. The antibodies can be stored at 2 degree C-8 degree C for three month without detectable loss of activity. Avoid repeated freezing-thawing cycles.

ELISA, Western Blot, Immunohistochemistry

Western Blot: 0.1-1 ug/ml. ELISA: 0.01-0.1 ug/ml. Immunoprecipitation: 2-5 ug/ml

Antigen Preparation: A synthetic peptide corresponding to the N-terminus of human IkBalpha protein. This sequence is identical within human, mouse, rat, dog and bovine.

Positive Control: TNFa-treated Jurkat cells

There are six members in the IkB family, in which IkBa is first protein induced by NF-kB activation. NF-kB is silenced in the cytoplasm by an inhibitory protein, IkB. Synthesis of IkBa is autoregulated. IkB proteins are phosphorylated by IkB kinase complex consisting of at least three proteins, IKK1/a, IKK2/b, and IKK3/g. External stimuli such as TNF or other cytokines initiates a signal transduction cascade that leads to the activation of IkB-kinase complex that specifically phosphorylates IkBa on Serine-32 and Serine-36. Phosphorylation of these sites leads to ubiquitination of IkBa and subsequent degradation by the 26 S proteasome.

Carole Kretz-Remy, et al. Inhibition of IKB-a Phosphorylation and Degradation and Subsequent NF-KB Activation by Glutathione Peroxidase Overexpression. (1996) The Journal of Cell Biology, 133 (5), 1083-1093.

6706211

P25963

~42 kDa

Activated TLR4 Signalling Pathway (106400); Adaptive Immunity Signaling Pathway (366160); Adipocytokine Signaling Pathway (83093); Adipocytokine Signaling Pathway (505); Apoptosis Pathway (198797); Apoptosis Pathway (83060); Apoptosis Pathway (470); Atypical NF-kappaB Pathway (137946); Aurora A Signaling Pathway (137925); B Cell Receptor Signaling Pathway (198909)

NFKB1 (MIM 164011) or NFKB2 (MIM 164012) is bound to REL (MIM 164910), RELA (MIM 164014), or RELB (MIM 604758) to form the NFKB complex. The NFKB complex is inhibited by I-kappa-B proteins (NFKBIA or NFKBIB, MIM 604495), which inactivate NF-kappa-B by trapping it in the cytoplasm. Phosphorylation of serine residues on the I-kappa-B proteins by kinases (IKBKA, MIM 600664, or IKBKB, MIM 603258) marks them for destruction via the ubiquitination pathway, thereby allowing activation of the NF-kappa-B complex. Activated NFKB complex translocates into the nucleus and binds DNA at kappa-B-binding motifs such as 5-prime GGGRNNYYCC 3-prime or 5-prime HGGARNYYCC 3-prime (where H is A, C, or T; R is an A or G purine; and Y is a C or T pyrimidine).[supplied by OMIM]

Function: Inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL dimers in the cytoplasm through masking of their nuclear localization signals. On cellular stimulation by immune and proinflammatory responses, becomes phosphorylated promoting ubiquitination and degradation, enabling the dimeric RELA to tranlocate to the nucleus and activate transcription. Ref.11. Subunit structure: Interacts with RELA; the interaction requires the nuclear import signal. Interacts with NKIRAS1 and NKIRAS2. Part of a 70-90 kDa complex at least consisting of CHUK, IKBKB, NFKBIA, RELA, IKBKAP and MAP3K14. Interacts with HBV protein X. Interacts with RWDD3; the interaction enhances sumoylation. Interacts (when phosphorylated at the 2 serine residues in the destruction motif D-S-G-X(2,3,4)-S) with BTRC. Associates with the SCF(BTRC) complex, composed of SKP1, CUL1 and BTRC; the association is mediated via interaction with BTRC. Part of a SCF(BTRC)-like complex lacking CUL1, which is associated with RELA; RELA interacts directly with NFKBIA. Interacts with PRMT2. Ref.10 Ref.19 Ref.21 Ref.24 Ref.25. Subcellular location: Cytoplasm. Nucleus. Note: Shuttles between the nucleus and the cytoplasm by a nuclear localization signal (NLS) and a CRM1-dependent nuclear export. By similarity. Ref.16 Ref.22 Ref.23 Ref.24. Induction: Induced in adherent monocytes. Post-translational modification: Phosphorylated; disables inhibition of NF-kappa-B DNA-binding activity. Phosphorylation at positions 32 and 36 is prerequisite to recognition by UBE2D3 leading to polyubiquitination and subsequent degradation. Ref.12 Ref.13 Ref.15 Ref.18 Ref.20Sumoylated; sumoylation requires the presence of the nuclear import signal. Ref.23 Ref.25Monoubiquitinated at Lys-21 and/or Lys-22 by UBE2D3. Ubiquitin chain elongation is then performed by CDC34 in cooperation with the SCF(FBXW11) E3 ligase complex, building ubiquitin chains from the UBE2D3-primed NFKBIA-linked ubiquitin. The resulting polyubiquitinatin leads to protein degredation. Also ubiquitinated by SCF(BTRC) following stimulus-dependent phosphorylation at Ser-32 and Ser-36.Deubiquitinated by porcine reproductive and respiratory syndrome virus Nsp2 protein, which thereby interefers with NFKBIA degradation and impairs subsequenbt NF-kappa-B activation. Involvement in disease: Defects in NFKBIA are the cause of ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant (ADEDAID) [. MIM:612132]. Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. ADEDAID is an ectodermal dysplasia associated with decreased production of pro-inflammatory cytokines and certain interferons, rendering patients susceptible to infection. Ref.30 Ref.31. Sequence similarities: Belongs to the NF-kappa-B inhibitor family.Contains 5 ANK repeats.

0.1 mg

250 USD