Product: Phospho-NF kappaB p105/p50 (Ser337) Antibody
Catalog: AF3219
Description: Rabbit polyclonal antibody to Phospho-NF kappaB p105/p50 (Ser337)
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 105,50kDa; 105kD(Calculated).
Uniprot: P19838
RRID: AB_2834647

View similar products>>

   Size Price Inventory
 100ul $280 In stock
 200ul $350 In stock

Lead Time: Same day delivery

For pricing and ordering contact:
Local distributors

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
Phospho-NF kappaB p105/p50 (Ser337) Antibody detects endogenous levels of NF kappaB p105/p50 only when phosphorylated at Serine 337.
RRID:
AB_2834647
Cite Format: Affinity Biosciences Cat# AF3219, RRID:AB_2834647.
Conjugate:
Unconjugated.
Purification:
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

DKFZp686C01211; DNA binding factor KBF1; DNA binding factor KBF1 EBP1; DNA-binding factor KBF1; EBP 1; EBP-1; EBP1; KBF1; MGC54151; NF kappa B; NF kappaB; NF kappabeta; NF kB1; NFkappaB; NFKB 1; NFKB p105; NFKB p50; Nfkb1; NFKB1_HUMAN; Nuclear factor kappa B DNA binding subunit; Nuclear factor kappa-B, subunit 1; Nuclear factor NF kappa B p105 subunit; Nuclear factor NF kappa B p50 subunit; Nuclear factor NF-kappa-B p50 subunit; Nuclear factor of kappa light chain gene enhancer in B cells 1; Nuclear factor of kappa light polypeptide gene enhancer in B cells 1; Nuclear factor of kappa light polypeptide gene enhancer in B-cells 1; p105; p50; p84/NF-kappa-B1 p98; Transcription factor NFKB1;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Description:
NFkB-p105 a transcription factor of the nuclear factor-kappaB ( NFkB) group. Undergoes cotranslational processing by the 26S proteasome to produce a 50 kD protein. The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of NFkB. NFkB is a transcription regulator that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products.
Sequence:
MAEDDPYLGRPEQMFHLDPSLTHTIFNPEVFQPQMALPTDGPYLQILEQPKQRGFRFRYVCEGPSHGGLPGASSEKNKKSYPQVKICNYVGPAKVIVQLVTNGKNIHLHAHSLVGKHCEDGICTVTAGPKDMVVGFANLGILHVTKKKVFETLEARMTEACIRGYNPGLLVHPDLAYLQAEGGGDRQLGDREKELIRQAALQQTKEMDLSVVRLMFTAFLPDSTGSFTRRLEPVVSDAIYDSKAPNASNLKIVRMDRTAGCVTGGEEIYLLCDKVQKDDIQIRFYEEEENGGVWEGFGDFSPTDVHRQFAIVFKTPKYKDINITKPASVFVQLRRKSDLETSEPKPFLYYPEIKDKEEVQRKRQKLMPNFSDSFGGGSGAGAGGGGMFGSGGGGGGTGSTGPGYSFPHYGFPTYGGITFHPGTTKSNAGMKHGTMDTESKKDPEGCDKSDDKNTVNLFGKVIETTEQDQEPSEATVGNGEVTLTYATGTKEESAGVQDNLFLEKAMQLAKRHANALFDYAVTGDVKMLLAVQRHLTAVQDENGDSVLHLAIIHLHSQLVRDLLEVTSGLISDDIINMRNDLYQTPLHLAVITKQEDVVEDLLRAGADLSLLDRLGNSVLHLAAKEGHDKVLSILLKHKKAALLLDHPNGDGLNAIHLAMMSNSLPCLLLLVAAGADVNAQEQKSGRTALHLAVEHDNISLAGCLLLEGDAHVDSTTYDGTTPLHIAAGRGSTRLAALLKAAGADPLVENFEPLYDLDDSWENAGEDEGVVPGTTPLDMATSWQVFDILNGKPYEPEFTSDDLLAQGDMKQLAEDVKLQLYKLLEIPDPDKNWATLAQKLGLGILNNAFRLSPAPSKTLMDNYEVSGGTVRELVEALRQMGYTEAIEVIQAASSPVKTTSQAHSLPLSPASTRQQIDELRDSDSVCDSGVETSFRKLSFTESLTSGASLLTLNKMPHDYGQEGPLEGKI

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Xenopus
100
Chicken
100
Rabbit
100
Zebrafish
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P19838 As Substrate

Site PTM Type Enzyme
S20 Phosphorylation P78527 (PRKDC)
Y59 Phosphorylation
C61 S-Nitrosylation
S65 Phosphorylation
S73 Phosphorylation
K148 Ubiquitination
Y165 Phosphorylation
S223 Phosphorylation
T228 Phosphorylation
Y240 Phosphorylation
S242 Phosphorylation
K243 Ubiquitination
K251 Ubiquitination
S301 Phosphorylation
T324 Phosphorylation
K325 Sumoylation
S328 Phosphorylation O14757 (CHEK1)
S337 Phosphorylation P17612 (PRKACA)
K345 Ubiquitination
Y409 Phosphorylation
T413 Phosphorylation
K431 Acetylation
K440 Acetylation
K440 Ubiquitination
K441 Acetylation
K441 Ubiquitination
S449 Phosphorylation
Y485 Phosphorylation
K504 Ubiquitination
Y582 Phosphorylation
T584 Phosphorylation
K624 Ubiquitination
K816 Ubiquitination
K821 Ubiquitination
K830 Ubiquitination
S851 Phosphorylation
S855 Phosphorylation
K856 Ubiquitination
T882 Phosphorylation
S892 Phosphorylation
S893 Phosphorylation
T897 Phosphorylation
S899 Phosphorylation
S903 Phosphorylation
S907 Phosphorylation
S910 Phosphorylation
T911 Phosphorylation
S923 Phosphorylation O15111 (CHUK) , O14920 (IKBKB)
S927 Phosphorylation O15111 (CHUK) , O14920 (IKBKB)
T931 Phosphorylation O15111 (CHUK)
S932 Phosphorylation O14920 (IKBKB) , O15111 (CHUK)
S937 Phosphorylation
T939 Phosphorylation
S941 Phosphorylation

Research Backgrounds

Function:

NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52 and the heterodimeric p65-p50 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric p65-p50 and RelB-p50 complexes are transcriptional activators. The NF-kappa-B p50-p50 homodimer is a transcriptional repressor, but can act as a transcriptional activator when associated with BCL3. NFKB1 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p105 and generation of p50 by a cotranslational processing. The proteasome-mediated process ensures the production of both p50 and p105 and preserves their independent function, although processing of NFKB1/p105 also appears to occur post-translationally. p50 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. In a complex with MAP3K8, NFKB1/p105 represses MAP3K8-induced MAPK signaling; active MAP3K8 is released by proteasome-dependent degradation of NFKB1/p105.

PTMs:

While translation occurs, the particular unfolded structure after the GRR repeat promotes the generation of p50 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.

Phosphorylation at 'Ser-903' and 'Ser-907' primes p105 for proteolytic processing in response to TNF-alpha stimulation. Phosphorylation at 'Ser-927' and 'Ser-932' are required for BTRC/BTRCP-mediated proteolysis.

Polyubiquitination seems to allow p105 processing.

S-nitrosylation of Cys-61 affects DNA binding.

The covalent modification of cysteine by 15-deoxy-Delta12,14-prostaglandin-J2 is autocatalytic and reversible. It may occur as an alternative to other cysteine modifications, such as S-nitrosylation and S-palmitoylation.

Subcellular Location:

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

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Subunit Structure:

Component of the NF-kappa-B p65-p50 complex. Component of the NF-kappa-B p65-p50 complex. Homodimer; component of the NF-kappa-B p50-p50 complex. Component of the NF-kappa-B p105-p50 complex. Component of the NF-kappa-B p50-c-Rel complex. Component of a complex consisting of the NF-kappa-B p50-p50 homodimer and BCL3. Also interacts with MAP3K8. NF-kappa-B p50 subunit interacts with NCOA3 coactivator, which may coactivate NF-kappa-B dependent expression via its histone acetyltransferase activity. Interacts with DSIPI; this interaction prevents nuclear translocation and DNA-binding. Interacts with SPAG9 and UNC5CL. NFKB1/p105 interacts with CFLAR; the interaction inhibits p105 processing into p50. NFKB1/p105 forms a ternary complex with MAP3K8 and TNIP2. Interacts with GSK3B; the interaction prevents processing of p105 to p50. NFKB1/p50 interacts with NFKBIE. NFKB1/p50 interacts with NFKBIZ. Nuclear factor NF-kappa-B p50 subunit interacts with NFKBID (By similarity). Directly interacts with MEN1. Interacts with HIF1AN.

Family&Domains:

The C-terminus of p105 might be involved in cytoplasmic retention, inhibition of DNA-binding, and transcription activation.

Glycine-rich region (GRR) appears to be a critical element in the generation of p50.

Research Fields

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Ras signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > cAMP signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > HIF-1 signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Sphingolipid signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Antifolate resistance.

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Substance dependence > Cocaine addiction.

· Human Diseases > Infectious diseases: Bacterial > Epithelial cell signaling in Helicobacter pylori infection.

· Human Diseases > Infectious diseases: Bacterial > Shigellosis.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis C.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Measles.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Transcriptional misregulation in cancer.

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

· Human Diseases > Cancers: Specific types > Pancreatic cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Prostate cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Acute myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Small cell lung cancer.   (View pathway)

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

· Organismal Systems > Immune system > Chemokine signaling pathway.   (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway.   (View pathway)

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > RIG-I-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Cytosolic DNA-sensing pathway.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Th1 and Th2 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > B cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Prolactin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

References

1). Genetic Arg-304-His substitution in GRK5 protects against sepsis progression by alleviating NF-κB-mediated inflammation. International Immunopharmacology, 2023 [IF=5.6]

2). Aspirin promotes apoptosis and inhibits proliferation by blocking G0/G1 into S phase in rheumatoid arthritis fibroblast-like synoviocytes via downregulation of JAK/STAT3 and NF-κB signaling pathway. INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 2018 (PubMed: 30221683) [IF=5.4]

Application: WB    Species: human    Sample: RA‑FLS cells

Figure 6. | Effects of aspirin on the NF‑κB signaling pathway. It was observed that aspirin significantly affects the phosphorylation levels of P65 and P50. (A) Cells were treated with various concentrations of aspirin for 24 h, and then whole cell lysates were obtained and subjected to western blotting to detect p‑P65, P65, p‑P50, P50, p‑P105 and P105. GAPDH served as the loading control. The levels of p‑P65 and p‑P50 decreased, whilst P65, P50, p‑P105 and P105 remained the same. Phosphorylation of P65 and P50 was inhibited to varying degrees by aspirin.

3). Integrating serum pharmacochemistry and network pharmacology to reveal the active constituents and mechanism of Corydalis Rhizoma in treating Alzheimer's disease. Frontiers in aging neuroscience, 2023 (PubMed: 38076535) [IF=4.8]

4). TIPE regulates DcR3 expression and function by activating the PI3K/AKT signaling pathway in CRC. Frontiers in Oncology, 2021 (PubMed: 33718119) [IF=4.7]

Application: WB    Species: Human    Sample: HCT116 cells

Figure 5 Tumor necrosis factor-induced protein-8 (TIPE)-mediated activation of the PI3K/Akt pathway is involved in the modulation of DcR3 levels in HCT116 cells. (A) HCT116 cells were transfected with TIPE or an empty vector (control) for 24 h with lipopolysaccharide (LPS) stimulation for the indicated time (0, 15, 30, and 60 min). Cells were harvested, and whole-cell extracts were prepared for Western blot analysis of the indicated proteins. The blots shown are representative of those obtained in three separate experiments. (B) HCT116 cells were cultured in 6-well plates and transfected with TIPE or an empty vector (control) for 24 h, then qRT-PCR assays were performed to measure the relative DcR3 mRNA expression of HCT116 cells after treatment with LY294002 (50 μM), NSC23766, U0126, and BAY 11-7082. Expression was normalized to that in the control cells. (C) The culture medium was collected, and DcR3 protein levels were measured by ELISA. (D) HCT116 cells were transfected with tumor necrosis factor-induced protein-8 (TIPE) after treatment with lipopolysaccharide (LPS) for the indicated time (0, 30, and 60 min), and Western blot analysis of whole-cell lysates was performed to examine the indicated proteins in HCT116 cells after treatment with or without LY294002 (50 μM). ns, not significant, *p < 0.05, ***p < 0.001.

5). Bradykinin protects against DDP-induced GP-H1 cell damage via activation of PI3K/Akt/NO signaling pathway. American Journal of Translational Research, 2023 (PubMed: 36915772) [IF=2.2]

6). Label-Free Quantitative Proteomic Profiling of LAD2 Mast Cell Releasates Reveals the Mechanism of Tween-80-Induced Anaphylactoid Reaction. Proteomics Clinical Applications, 2020 (PubMed: 32012444) [IF=2.0]

Application: WB    Species: human    Sample: LAD2 mast cells

Figure 5.| Differentially quantified proteins from the releasates of Tween-80-stimulated LAD2 mast cells involved in NF-𝜅B signaling pathway. A) Green shows the differentially quantified proteins in NF-𝜅B signaling pathway; B) abundances of proteins involved in NF-𝜅B signaling pathway. C) Western blotting verification of P105 and P65. n = 3 or 5. *p < 0.05, versus control.

Restrictive clause

 

Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.

For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.