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  • Product Name
    NF-kB p65 Antibody
  • Catalog No.
  • RRID
  • Source
  • Application
  • Reactivity
    Human, Mouse, Rat, Monkey
  • Prediction
    Pig, Bovine, Horse, Sheep, Dog
  • UniProt
  • Mol.Wt
  • Concentration
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Product Information

Alternative Names:Expand▼

Avian reticuloendotheliosis viral (v rel) oncogene homolog A; MGC131774; NF kappa B p65delta3; NFKB3; Nuclear Factor NF Kappa B p65 Subunit; Nuclear factor NF-kappa-B p65 subunit; Nuclear factor of kappa light polypeptide gene enhancer in B cells 3; Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3; OTTHUMP00000233473; OTTHUMP00000233474; OTTHUMP00000233475; OTTHUMP00000233476; OTTHUMP00000233900; p65; p65 NF kappaB; p65 NFkB; relA; TF65_HUMAN; Transcription factor p65; v rel avian reticuloendotheliosis viral oncogene homolog A (nuclear factor of kappa light polypeptide gene enhancer in B cells 3 (p65)); V rel avian reticuloendotheliosis viral oncogene homolog A; v rel reticuloendotheliosis viral oncogene homolog A (avian); V rel reticuloendotheliosis viral oncogene homolog A, nuclear factor of kappa light polypeptide gene enhancer in B cells 3, p65;


WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:200, ELISA(peptide) 1:20000-1:40000
*The optimal dilutions should be determined by the end user.


Human, Mouse, Rat, Monkey

Predicted Reactivity:

Pig, Bovine, Horse, Sheep, Dog






The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).


NF-kB p65 Antibody detects endogenous levels of total NF-kB p65.


Please cite this product as: Affinity Biosciences Cat# AF5006, RRID:AB_2834847.





Storage Condition and Buffer:

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.

Immunogen Information in 3D


A synthesized peptide derived from human NF-kB p65, corresponding to a region within C-terminal amino acids.


>>Visit The Human Protein Atlas

Gene ID:

Gene Name:


Molecular Weight:

Observed Mol.Wt.: 65~80kD.
Predicted Mol.Wt.: 60kDa(Calculated)..

Subcellular Location:

Nucleus. Cytoplasm. Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B). Colocalized with RELA in the nucleus upon TNF-alpha induction.


NFKB1 (MIM 164011) or NFKB2 (MIM 164012) is bound to REL (MIM 164910), RELA, or RELB (MIM 604758) to form the NFKB complex. The p50 (NFKB1)/p65 (RELA) heterodimer is the most abundant form of NFKB. The NFKB complex is inhibited by I-kappa-B proteins (NFKBIA, MIM 164008 or NFKBIB, MIM 604495), which inactivate NFKB by trapping it in the cytoplasm.


Research Background


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. The heterodimeric RELA-NFKB1 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. The NF-kappa-B heterodimeric RELA-NFKB1 and RELA-REL complexes, for instance, function as transcriptional activators. 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. The inhibitory effect of I-kappa-B on NF-kappa-B through retention in the cytoplasm is exerted primarily through the interaction with RELA. RELA shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Beside its activity as a direct transcriptional activator, it is also able to modulate promoters accessibility to transcription factors and thereby indirectly regulate gene expression. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Essential for cytokine gene expression in T-cells. The NF-kappa-B homodimeric RELA-RELA complex appears to be involved in invasin-mediated activation of IL-8 expression.

Post-translational Modifications:

Ubiquitinated by RNF182, leading to its proteasomal degradation. Degradation is required for termination of NF-kappa-B response.

Monomethylated at Lys-310 by SETD6. Monomethylation at Lys-310 is recognized by the ANK repeats of EHMT1 and promotes the formation of repressed chromatin at target genes, leading to down-regulation of NF-kappa-B transcription factor activity. Phosphorylation at Ser-311 disrupts the interaction with EHMT1 without preventing monomethylation at Lys-310 and relieves the repression of target genes (By similarity).

Phosphorylation at Ser-311 disrupts the interaction with EHMT1 and promotes transcription factor activity (By similarity). Phosphorylation on Ser-536 stimulates acetylation on Lys-310 and interaction with CBP; the phosphorylated and acetylated forms show enhanced transcriptional activity. Phosphorylation at Ser-276 by RPS6KA4 and RPS6KA5 promotes its transactivation and transcriptional activities.

Reversibly acetylated; the acetylation seems to be mediated by CBP, the deacetylation by HDAC3 and SIRT2. Acetylation at Lys-122 enhances DNA binding and impairs association with NFKBIA. Acetylation at Lys-310 is required for full transcriptional activity in the absence of effects on DNA binding and NFKBIA association. Acetylation at Lys-310 promotes interaction with BRD4. Acetylation can also lower DNA-binding and results in nuclear export. Interaction with BRMS1 promotes deacetylation of Lys-310. Lys-310 is deacetylated by SIRT2.

S-nitrosylation of Cys-38 inactivates the enzyme activity.

Sulfhydration at Cys-38 mediates the anti-apoptotic activity by promoting the interaction with RPS3 and activating the transcription factor activity.

Sumoylation by PIAS3 negatively regulates DNA-bound activated NF-kappa-B.

Proteolytically cleaved within a conserved N-terminus region required for base-specific contact with DNA in a CPEN1-mediated manner, and hence inhibits NF-kappa-B transcriptional activity.

Subcellular Location:

Nucleus. Cytoplasm.
Note: Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B) (PubMed:1493333). Colocalized with DDX1 in the nucleus upon TNF-alpha induction (PubMed:19058135). Colocalizes with GFI1 in the nucleus after LPS stimulation (PubMed:20547752). Translocation to the nucleus is impaired in L.monocytogenes infection (PubMed:20855622).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionGraphics by Christian Stolte

Subunit Structure:

Component of the NF-kappa-B p65-p50 complex. Component of the NF-kappa-B p65-c-Rel complex. Homodimer; component of the NF-kappa-B p65-p65 complex. Component of the NF-kappa-B p65-p52 complex. May interact with ETHE1. Binds TLE5 and TLE1. Interacts with TP53BP2. Binds to and is phosphorylated by the activated form of either RPS6KA4 or RPS6KA5. Interacts with ING4 and this interaction may be indirect. Interacts with CARM1, USP48 and UNC5CL. Interacts with IRAK1BP1 (By similarity). Interacts with NFKBID (By similarity). Interacts with NFKBIA. Interacts with GSK3B. Interacts with NFKBIB (By similarity). Interacts with NFKBIE. Interacts with NFKBIZ. Interacts with EHMT1 (via ANK repeats) (By similarity). Part of a 70-90 kDa complex at least consisting of CHUK, IKBKB, NFKBIA, RELA, ELP1 and MAP3K14. Interacts with HDAC3; HDAC3 mediates the deacetylation of RELA. Interacts with HDAC1; the interaction requires non-phosphorylated RELA. Interacts with CBP; the interaction requires phosphorylated RELA. Interacts (phosphorylated at 'Thr-254') with PIN1; the interaction inhibits p65 binding to NFKBIA. Interacts with SOCS1. Interacts with UXT. Interacts with MTDH and PHF11. Interacts with ARRB2. Interacts with NFKBIA (when phosphorylated), the interaction is direct; phosphorylated NFKBIA is part of a SCF(BTRC)-like complex lacking CUL1. Interacts with RNF25. Interacts (via C-terminus) with DDX1. Interacts with UFL1 and COMMD1. Interacts with BRMS1; this promotes deacetylation of 'Lys-310'. Interacts with NOTCH2 (By similarity). Directly interacts with MEN1; this interaction represses NFKB-mediated transactivation. Interacts with AKIP1, which promotes the phosphorylation and nuclear retention of RELA. Interacts (via the RHD) with GFI1; the interaction, after bacterial lipopolysaccharide (LPS) stimulation, inhibits the transcriptional activity by interfering with the DNA-binding activity to target gene promoter DNA. Interacts (when acetylated at Lys-310) with BRD4; leading to activation of the NF-kappa-B pathway. Interacts with MEFV. Interacts with CLOCK (By similarity). Interacts (via N-terminus) with CPEN1; this interaction induces proteolytic cleavage of p65/RELA subunit and inhibition of NF-kappa-B transcriptional activity. Interacts with FOXP3. Interacts with CDK5RAP3; stimulates the interaction of RELA with HDAC1, HDAC2 and HDAC3 thereby inhibiting NF-kappa-B transcriptional activity. Interacts with DHX9; this interaction is direct and activates NF-kappa-B-mediated transcription. Interacts with LRRC25. Interacts with TBX21 (By similarity). Interacts with KAT2A (By similarity). Interacts with ZBTB7A; involved in the control by RELA of the accessibility of target gene promoters. Directly interacts with DDX3X; this interaction may trap RELA in the cytoplasm, impairing nuclear relocalization upon TNF activating signals.

(Microbial infection) Interacts with human respiratory syncytial virus (HRSV) protein M2-1.

(Microbial infection) Interacts with molluscum contagiosum virus MC132.

(Microbial infection) Interacts with herpes virus 8 virus protein LANA1.


The transcriptional activation domain 3/TA3 does not participate to the direct transcriptional activity of RELA but is involved in the control by RELA of the accessibility of target gene promoters. Mediates interaction with ZBTB7A.

The transcriptional activation domain 1/TA1 and the transcriptional activation domain 2/TA2 have direct transcriptional activation properties (By similarity). The 9aaTAD motif found within the transcriptional activation domain 2 is a conserved motif present in a large number of transcription factors that is required for their transcriptional transactivation activity (PubMed:17467953).

Research Fields

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: 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.

WB Images(11)

IHC Images(1)

IF/ICC Images(1)

Reference Citations:

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Application: WB    Species:mouse;    Sample:liver

Figure 7. Effect of A22 on ameliorating apoptosis, ER stress, inflammation, metabolic syndrome, and fibrogenesis in HF diet-fed mice. (A) Effect of A22 on BCL-2 gene transcription. (B) Effect of A22 on BAX gene transcription. (C) Effect of A22 on expressions of apoptosis-related proteins in liver. The extracted proteins from the liver were immunoblotted with specific antibodies, and quantified based on the loading control of ACTIN. (D) Effect of A22 on ER stress. The UPR proteins (IRE-1, PERK, elF-2 and CHOP) were analyzed by using western Blot. (E) Effect of A22 on expressions of inflammatory factors. (F) Effect of A22 on expressions of fibrogenic proteins.

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Application: IHC    Species:human;    Sample:Not available

Figure 2. PnAg promotes wound healing in SD rats. (A) Photographs of rat skin full-thickness excision wounds on different post-excision days. (B) Change in wound areas of SD rats after treatment; (C) and (D) Expression levels of collagen I, NF-κB, TGF-ß, MMP-2, and MMP-9 in tissues on day 7 and 17 detected by immunohistochemistry. (E) Histogram of protein expression levels in these tissues. (F) and (G) Histomorphological changes in wound tissues stained by Masson trichrome and HE on day 17.

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Application: WB    Species:mouse;    Sample:Not available

Fig. 9. FGF21 displayed the similar effects with Adalimumab in improving RA partly by inhibiting NF-kB/IkBa signaling pathway. The CIA mice were randomly divided into 3 groups and un-induced mice were regarded as healthy controls. CIA mice were treated with saline (0.9%), FGF21 (1 mg/kg) or Adalimumab (1 mg/kg) once a day. The spleens were collected and analyzed for determining the protein expression levels of NF-kB p65, IkBa and IKKb by western blotting. (A) Western blotting analysis of NF-kB p65 in the nuclear of the spleen. The relative level of NF-kB p65 was expressed as the ratio NF-kB p65/Lamin b1.

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Application: WB    Species:rat;    Sample:Not available

FIGURE 3: Pro-inflammatory factors, anti-oxidant enzyme and cell signaling pathways in resveratrol (Res)- or vehicle-treated cystic kidneys. (A) TNF-α, MCP-1, CFB and SOD2 were analyzed by western blot in 9-week-old +/+ and Cy/+ kidneys. (B–E) Immunohistochemical staining for oxidative stress markers 8-OHdG and nitrotyrosine in the tubulointerstitial area. Computer-assisted morphometry was used to quantify changes of 8-OHdG and nitrotyrosine in each group. Scale bar = 50 µm. (F) NF-κB pathway ( p-p65, p65, p105 and p50) and mTOR pathway ( p-S6K and total S6K) were analyzed by western blot in 9-week-old +/+ and Cy/+ kidneys. Blots are representative of three independent experiments.

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Application: WB    Species:Not available;    Sample:Not available

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79). Zhu G et al. MyD88 Regulates LPS-induced NF-ĸB/MAPK Cytokines and Promotes Inflammation and Malignancy in Colorectal Cancer Cells. Cancer Genomics Proteomics 2019 Nov-Dec;16(6):409-419 (PubMed: 31659096) [IF=3.280]

80). Wu Q et al. The bispecific antibody aimed at the vicious circle of IL-1β and IL-17A, is beneficial for the collagen-induced rheumatoid arthritis of mice through NF-κB signaling pathway. Immunol Lett 2016 Nov;179:68-79 (PubMed: 27616043) [IF=3.276]

Application: WB    Species:mouse;    Sample:Not available

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Application: WB    Species:mouse;    Sample:mouse brain

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Application: WB    Species:human;    Sample:human lung adenocarcinoma cells

Fig. 2 Overexpression of RBM5 induced cell autophagy-related protein expression. A549 cells were treated with RBM5 overexpression (RBM5 group), control plasmids (control group), or RBM5 overexpression combined with 3-MA (RBM5+3-MA group). a Western blot analysis of the protein expression levels of LC3-I, LC3-II, LAMP1, and β-actin in A549 cells. b Quantification of protein expression relative to β-actin. c Quantification of LC3-II expression relative to LC3-I. d Western blot analysis of the protein expression levels of NF-κB/p65, Bcl-2, Beclin1, and β-actin in A549 cells. e Quantification of protein expression relative to β-actin. Data shown are representative of three independent experiments and presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001

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Application: WB    Species:human;    Sample:HGC27

Figure 4 CUL4A and NF-κB were overexpressed in GC tissues. Notes: (A) Representative images of gastric tumor tissues showing concordant positive staining of CUL4A and NF-κB in the same sample (200×). (B) Western blot analysis of CUL4A and NF-κB expressions in three paired primary GC and adjacent noncancerous tissue samples. These three patients were all diagnosed stage III. (C) CUL4A expression scores and NF-κB expression scores in 50 GC samples revealed that CUL4A expression positively correlated with NF-κB expression via correlation analysis

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Catalog Number :

(Blocking peptide available as AF5006-BP)

Price/Size :

Tips: For phospho antibody, we provide phospho peptide(0.5mg) and non-phospho peptide(0.5mg).

Function :

Blocking peptides are peptides that bind specifically to the target antibody and block antibody binding. These peptide usually contains the epitope recognized by the antibody. Antibodies bound to the blocking peptide no longer bind to the epitope on the target protein. This mechanism is useful when non-specific binding is an issue, for example, in Western blotting (immunoblot) and immunohistochemistry (IHC). By comparing the staining from the blocked antibody versus the antibody alone, one can see which staining is specific; Specific binding will be absent from the western blot or immunostaining performed with the neutralized antibody.

Format and storage :

Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 10 mg/ml.The purity is >90%,tested by HPLC and MS.Storage Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.

Precautions :

This product is for research use only. Not for use in diagnostic or therapeutic procedures.

High similarity Medium similarity Low similarity No similarity
Q04206 as Substrate
Site PTM Type Enzyme
M1 Acetylation
K37 Methylation
K37 Sumoylation
C38 S-Nitrosylation
S42 Phosphorylation
S45 Phosphorylation
K56 Ubiquitination
K62 Ubiquitination
T71 Phosphorylation
S75 Phosphorylation
K79 Ubiquitination
K93 Ubiquitination
S112 Phosphorylation
K122 Acetylation
K122 Ubiquitination
K123 Acetylation
K123 Ubiquitination
S131 Phosphorylation
T136 Phosphorylation
R174 Methylation
S180 Phosphorylation
R187 Methylation
K195 Ubiquitination
S205 Phosphorylation
K218 Acetylation
K218 Methylation
K218 Ubiquitination
K221 Acetylation
K221 Methylation
S238 Phosphorylation
S240 Phosphorylation
T254 Phosphorylation
S261 Phosphorylation
S269 Phosphorylation
S276 Phosphorylation P11309 (PIM1) , O94806 (PRKD3) , O75676 (RPS6KA4) , P17612 (PRKACA) , O75582 (RPS6KA5)
S281 Phosphorylation
T305 O-Glycosylation
T305 Phosphorylation
Y306 Phosphorylation
T308 Phosphorylation
K310 Acetylation
K310 Methylation
K310 Ubiquitination
S311 Phosphorylation Q05513 (PRKCZ)
K314 Acetylation
K314 Methylation
K314 Ubiquitination
K315 Acetylation
K315 Methylation
K315 Ubiquitination
S316 Phosphorylation P48729 (CSNK1A1)
S319 O-Glycosylation
T322 O-Glycosylation
S337 O-Glycosylation
S337 Phosphorylation
T352 O-Glycosylation
S374 O-Glycosylation
S374 Phosphorylation
S377 O-Glycosylation
T429 Phosphorylation
T435 Phosphorylation P28482 (MAPK1)
S468 Phosphorylation P49841 (GSK3B) , O14920 (IKBKB) , Q14164 (IKBKE)
S472 Phosphorylation
T505 Phosphorylation
S529 Phosphorylation P68400 (CSNK2A1) , P47710 (CSN1S1)
S536 Phosphorylation O15111 (CHUK) , O94806 (PRKD3) , Q9Y6K9 (IKBKG) , Q9UHD2 (TBK1) , Q9HCP0 (CSNK1G1) , Q16566 (CAMK4) , P51812 (RPS6KA3) , Q15418 (RPS6KA1) , Q00534 (CDK6) , O14920 (IKBKB) , P24723 (PRKCH) , Q14164 (IKBKE)
S543 Phosphorylation P68400 (CSNK2A1)
S547 Phosphorylation Q13315 (ATM)
IMPORTANT: For western blots, incubate membrane with diluted antibody in 5% w/v milk , 1X TBS, 0.1% Tween®20 at 4°C with gentle shaking, overnight.

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