Milli-Mark® Anti-NFκB p52-FITC

Milli-Mark® Anti-NFκB p52-FITC Antibody | FCMAB346F

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This antibody recognizes the p52 subunit of NFκB and its p100 precursor.

97 kDa Calculated

GST-fusion protein corresponding to amino acids 1-444 of human NFκB p52 subunit (Schmidt, R., 1991;Bours, V., 1992).

IgG2a

The NFκB transcription factor was originally identified as a protein complex consisting of a DNA binding subunit and an associated protein. The DNA binding subunit is functionally related to c-Rel p75 and Rel B p68. The p50 subunit was initially believed to be a functionally unique protein derived from the amino terminus of a precursor designated p105. A cDNA has been isolated that encodes an alternative DNA binding subunit of NFκB. It is synthesized as a protein that is expressed in a variety of cell types and, like p105, undergoes cleavage to generate its NFκB subunit, in this case a protein designated p52 (previously referred to as p49). In contrast to p50 derived from p105, p52 acts in synergy with p65 to stimulate the HIV enhancer in transiently transfected Jurkat cells.

Human

Tested and passed on Human. Does not cross-react with mouse or rat; other species cross-reactivity is unknown.

HeLa cells

Evaluated by flow cytometry using HeLa cells.

Protein G Purified

Purified mouse monoclonal IgG2a conjugated to FITC in PBS with 0.1% sodium azide and 15 mg/mL BSA.

Maintain refrigerated at 2-8 °C protected from light in undiluted aliquots for up to 6 months from date of receipt.

Q9WTK5

NP_062281

• NFKB2
• LYT10
• H2TF1
• LYT-10
• Lyt10

• DNA-binding factor KBF2
• Lymphocyte translocation chromosome 10
• Oncogene Lyt-10
• nuclear factor of kappa light chain gene enhancer in B-cells 2 (p49/p100)

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.

Flow Cytometry

NFKB has been detected in numerous cell types that express cytokines, chemokines, growth factors, cell adhesion molecules, and some acute phase proteins in health and in various disease states. NFKB is activated by a wide variety of stimuli such as cytokines, oxidant-free radicals, inhaled particles, ultraviolet irradiation, and bacterial or viral products. Inappropriate activation of NF-kappa-B has been linked to inflammatory events associated with autoimmune arthritis, asthma, septic shock, lung fibrosis, glomerulonephritis, atherosclerosis, and AIDS. In contrast, complete and persistent inhibition of NF-kappa-B has been linked directly to apoptosis, inappropriate immune cell development, and delayed cell growth. For reviews, see Chen et al. (1999) [PubMed 9895331] and Baldwin (1996) [PubMed 8717528].[supplied by OMIM] .

FUNCTION: SwissProt: Q00653 # Appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins and generation of p52 by a cotranslational processing. The proteasome-mediated process ensures the production of both p52 and p100 and preserves their independent function. p52 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. p52 and p100 are respectively the minor and major form; the processing of p100 being relatively poor. Isoform p49 is a subunit of the NF-kappa-B protein complex, which stimulates the HIV enhancer in synergy with p65.

SIZE: 900 amino acids; 96749 Da

SUBUNIT: Active NF-kappa-B is a heterodimer of an about 52 kDa DNA-binding subunit and the weak DNA-binding subunit p65. Two heterodimers might form a labile tetramer.

SUBCELLULAR LOCATION: Nucleus. Cytoplasm. Note=Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B).

DOMAIN: SwissProt: Q00653 The C-terminus of p100 might be involved in cytoplasmic retention, inhibition of DNA-binding by p52 homodimers, and/or transcription activation (By similarity). & The glycine-rich region (GRR) appears to be a critical element in the generation of p52.

PTM: While translation occurs, the particular unfolded structure after the GRR repeat promotes the generation of p52 making it an acceptable substrate for the proteasome. This process is known as cotranslational processing. The processed form is active and the unprocessed form acts as an inhibitor (I kappa B-like), being able to form cytosolic complexes with NF-kappa B, trapping it in the cytoplasm. Complete folding of the region downstream of the GRR repeat precludes processing. & Subsequent to MAP3K14-dependent serine phosphorylation, p100 polyubiquitination occurs then triggering its proteasome-dependent processing. & Constitutive processing is tightly suppressed by its C- terminal processing inhibitory domain, named PID, which contains the death domain.

DISEASE: SwissProt: Q00653 # A chromosomal aberration involving NFKB2 is found in a case of B-cell non Hodgkin lymphoma (B-NHL). Translocation t(10;14)(q24;q32) with IGHA1. The resulting oncogene is also called Lyt-10C alpha variant. & A chromosomal aberration involving NFKB2 is found in a cutaneous T-cell leukemia (C-TCL) cell line. This rearrangement produces the p80HT gene which encodes for a truncated 80 kDa protein (p80HT). & In B-cell leukemia (B-CLL) cell line, LB40 and EB308, can be found after heterogeneous chromosomal aberrations, such as internal deletions.

SIMILARITY: Contains 7 ANK repeats. & Contains 1 death domain. & Contains 1 RHD (Rel-like) domain.

Milli-Mark® Anti-NFκB p52-FITC

Monoclonal Antibody

100 tests

FITC

Mouse