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Validated All-in-One™ qPCR Primer for RELA(NM_021975.3) Search again
Product ID:
HQP108589
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AIF3BL3, CMCU, NFKB3, p65
Gene Description:
RELA proto-oncogene, NF-kB subunit
Target Gene Accession:
NM_021975.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
NFKB1 (MIM 164011) or NFKB2 (MIM 164012) is bound to REL (MIM 164910), RELA, or RELB (MIM 604758) to form the NFKB complex.
Gene References into function
- Physical exercise induces activation of NF-kappaB in human peripheral blood lymphocytes
- Respiratory syncytial virus induction of chemokine gene expression involves a redox-sensitive NF-kappaB1 signaling mechanism that differs from that mediated by TNF alpha in that it involves predominantly the RelA subunit of NF-kappaB.
- activation and expression of nuclear factor-kappaB (NF-kappaB) and effects of anti-inflammatory treatment on NF-kappaB in the intestinal mucosa of patients with ulcerative colitis (UC)
- MDM2 can induce expression of the p65 subunit of NF-kappaB
- NF-KB could be considered as a coordinating element in the body's response to stress, infection or inflammation, and it may be a good therapeutic target.
- A novel form is induced by and forms a complex with the proto-oncogene c-Myc
- NFkB is associated with antiestrogen resistance in breast cancer
- C-Rel can both induce and inhibit apoptosis in HeLa cells by upregulation of MnSOD
- NF-kappaB is regulated by the redox factor Ref-1 in the nucleus
- Data show that interleukin-1 induces nuclear transport of RelA.
- cross-linking FcgammaRI and -RII but not FcgammaRIII activates transcription factor NF-kappaB(p65)
- acetylation of p65 plays a key role in IkappaBetaalpha-mediated attenuation of NF-kappaBeta transcriptional activity which is an important process that restores the latent state in post-induced cells
- The NF-kappa B activation in lymphotoxin beta receptor signaling depends on the phosphorylation of p65 at serine 536.
- B-oligomer of pertussis toxin inhibits HIV-1 LTR-driven transcription through suppression of NF-kappaB p65 subunit activity
- Protein kinase C delta-NF-kappaB signaling regulates VCAM1 stimulation by thrombin in endothelial cells
- RelA expression is regulated by replication factor C (p140)
- mediates tumor necrosis factor alpha-induced nuclear translocation of telomerase reverse transcriptase protein
- S276 is the major phosphorylation site of p65 and its phosphorylation is essential for p65-dependent cellular responses
- IkappaBalpha and p65 have roles in regulating the cytoplasmic shuttling of nuclear corepressors
- The translocation of RelA/p65 was investigated using Western blotting and immunocytochemistry. the COX-2 inhibitor SC236 worked directly through suppressing nuclear translocation of RelA/p65.
- Adenosine selectively suppresses TNF-induced NF-kappaB activation, which may contribute to its role in suppression of inflammation and of the immune system.
- Inhibiting constitutive NF-kappa B activity by expressing I kappa B alpha M suppressed the tumorigenicity of a nonmetastatic human pancreatic cancer cell line, PANC-1, in an orthotopic nude mouse model.
- Data show that increased expression of nuclear factor-kappaB (NF-kB) in amnion during labor is associated with an increase in the expression of NF-kBp65 and the NF-kB binding proteins IkBa, IkBb-1 and IkBb-2.
- NF-kappa B induced proinflammatory & antiapoptotic genes in epithelial and mesenchymal cells of human skin. In keratinocytes, not fibroblasts, it induced p21(CIP1). GIF levls increased by NF-kappa B in both, but inhibited growth only in keratinocytes.
- NF-kappaB has a role in the migration and the organ-specific homing of metastatic breast cancer cells
- p65/RelA, one of the two subunits of the transcription factor NF-kappaB, binds to the BRCA1 protein.
- SINK specifically interacted with the NF-kappaB transactivator p65 and inhibited p65 phosphorylation
- RING finger protein AO7 supports NF-kappaB-mediated transcription by interacting with the transactivation domain of the p65 subunit.
- Mitogenic and antiapoptotic role of constitutive NF-kappaB/Rel activity in pancreatic cancer.
- During dendritic cell maturation, rapidly activated dimers (e.g.,RelA) bound to a subset of target promoters are gradually replaced by slowly activated dimers (e.g., RelB).
- Primary CML blasts showed constitutive p65/RelA NF-kappaB/Rel DNA binding activity
- IkappaB and NF-kappaB are substrates for the IKK complex in the activation of NF-kappaB
- NFkB confers estrogen-independent growth on breast cancer
- NFkB is part of a gene network impliceted in estrogen receptor signaling
- Ciglitazone induced phosphorylation of PPARgamma through the MAP kinase pathway provides a potential regulatory mechanism for PPARgamma's physical interaction with p65
- STAT3/NF-kappaB p65 cross-talk activated by IL-1 via TRAF6.
- TGF-beta1 is a negative regulator of NF-kappaB p65 activation in the gut
- overexpression of TNF-alpha downstream signaling targets, nuclear factor-kappaB (NF-kappaB)-inducing kinase (NIK) and p65 nuclear factor NF-kappaB, lowers PTEN expression
- RelA blunts IL-4 induction in T cells during the relapse in patients with minimal change nephrotic syndrome.
- Data show that NF-kappaB function is regulated by Pin1-mediated prolyl isomerization and ubiquitin-mediated proteolysis of its p65/RelA subunit.
- the p65 peptide that can selectively inhibit NF-kappaB activation induced by various inflammatory stimuli, down-regulate NF-kappaB-mediated gene expression, and up-regulate apoptosis
- NF-kappaBp65 and hTERT expressions are upregulated at the early stage of gastric carcinogenesis.
- Intestinal type gastric carcinoma is strongly associated with high expression of c-myc, cyclinD1 and bcl-xl through NF-kappaB/p65 activated by H pylori cagA
- NF-kappaB positively regulates the NR1 promoter during neuronal differentiation via interacting mainly with Sp1/Sp3
- RelA expression is altered in metastatic melanoma cells and has a role in deregulated NFkappaB signaling
- NF-kappaB p65 Thr dephosphorylation is activated by protein phosphatase 4
- NF-kappaB activation is induced by p53 by an IkappaB kinase-independent mechanism involving phosphorylation of p65 by ribosomal S6 kinase 1
- transcription of CD28-induced genes is mediated by the specific recruitment of RelA and p52 NF-kappaB subunits to target promoters
- Jurkat T cell costimulation-induced phosphorylation sites have been systematically mapped within the carboxyl-terminal half of the strongly trans-activating NF-kappa B p65 subunit; serine 536 is identified as the main phosphorylation site.
- Ang II stimulates IL-6 and IL-8 production and release from human adipocytes by a NF-kappaB-dependent pathway. Ang II increases p50/p65 heterodimer translocation to the nucleus in adipocytes.
- the transcriptional activity of p65 is suppressed by PIAS3
- unique mechanism for p53 regulation by the p65/RelA subunit of NF-kappaB.
- IVIG inhibits NF-kappaB activation induced by TNF-alpha in cultured endothelial cells of coronary arteries, thereby possibly modulating IL-6 production and E-selectin expression
- The decrease of NF-kappaB p65 subunit and up-regulation of IL-2 are potential mechanism of glucocorticoid resistance in steroid-resistant nephrotic syndrome.
- These results indicate that proteasomal degradation of p65/RelA does not merely regulate its stability and abundance, but also actively promotes transcriptional termination.
- mitochondrial recruitment of NF-kappaB observed following ANT1 overexpression has an important role in ANT1 proapoptotic activity
- cAMP concentration in endothelial cells prevents thrombin-induced ICAM-1 expression by inhibiting p38 MAPK activation, which in turn prevents phosphorylation of RelA/p65 and transcriptional activity of the bound NF-kappaB.
- NF-kappaB/p65 is constitutively activated in human prostate adenocarcinoma and is related to tumor progression.
- increased expression of RelA/nuclear factor-kappaB plays an important role in the pathogenesis of colorectal carcinoma.
- IL-1-inducible phosphorylation of p65 NFkB is mediated by multiple protein kinases including IKKalpha, IKKbeta, IKKepsilon, TBK1, and an unknown kinase and couples p65 to TAFII31-mediated IL-8 transcription
- TRAIL effects on mitochondrial NF-kappaB-DNA binding
- transcription of target genes depended on oscillation persistence, involving cycles of RelA phosphorylation and dephosphorylation
- a signal-specific transcriptional repression appears to selectively inhibit stimuli that transiently activate p65-p50 complexes
- the p65-dependent repression and the E1A-mediated attenuation of repression require the Brg1-dependent chromatin remodeling function and p300/CBP-dependent complex formation at a promoter assembled within chromatin
- data demonstrate, for the first time to our knowledge, that the RAGE-NF-kappaB axis operates in diabetic neuropathy, by mediating functional sensory deficits, and that its inhibition may provide new therapeutic approaches
- Inhibition of NFkB restores sensitivity to antiestrogens
- Plk3 is a RelA-NF-kappaB-regulated gene that induces apoptosis in both p53-dependent and -independent signaling pathways
- NF-kappaB RelA (p65) activation was related with increased heparanase gene expression and correlated with poor clinicopathological characteristics in gastric cancers
- Shear stress inhibited the smooth muscle cell coculture-induced NF-kappaB activation in endothelial cells and monocytic THP-1 cell adhesion to ECs.
- caspase-8 deficiency specifically abolishes activation of NF-kappaB after stimulation in T, B & NK cells; recruitment of the IKKalpha, beta complex, its activation & the nuclear translocation of NF-kappaB require activity of full-length caspase-8
- inactivation of NF-kappaB function by proteolytic cleavage of p65-RelA is the common mechanism by which picornaviruses suppress the innate immune response
- transactivation and phosphorylation on serine 536 is mediated by bruton's tyrosine kinase
- the constitutive activation and the protein expression of NF-kappaB are different in gastric cancer cell lines
- whereas wild type p16INK4a strongly inhibits NF-kappaB transcriptional activity, a subset of melanoma-associated p16INK4a mutants show reduced NF-kappaB inhibitory function
- FBI-1 enhances transcription of the NF-kappaB-responsive E-selectin gene by nuclear localization of the p65 subunit of NF-kappaB
- data support the notion that PKCzeta is essential for LPS-induced NF-kB p65 subunit nuclear translocation in human myometrial cells
- NF-kappaB may regulate Fas-mediated apoptosis in HIVAN by controlling the expression of Fas ligand in renal epithelium
- The nucleolar accumulation of RelA is paralleled by a decrease in basal levels of NF-kappaB transcriptional activity and by apoptosis.
- Upon neutrophil activation, RelA becomes phosphorylated in both cell nucleus and cytoplasm
- IKKbeta phosphorylates multiple p65 sites, as well as in an IkappaB-p65 complex, and S468 phosphorylation slightly reduces TNF-alpha- and IL-1beta-induced NF-kappaB activation
- Data show that stimulation of PAR1 results in increased DNA binding of the NFkappaB p65 subunit, and that activation of PAR1 attenuates docetaxel induced apoptosis through the upregulation of Bcl-xL.
- RelA did not bind directly to the Galphas promoter. Expression of a coactivator protein, cAMP response element binding protein binding protein, relieved RelA-induced down-regulation of Galphas. expression.
- p65 phosphorylated on serine 536 is not associated with or regulated by IkappaBalpha, but it has a distinct set of target genes and may represent a noncanonical NF-kappaB pathway that is independent of IkappaBalpha regulation
- Acetylation of RelA at lysine 310 is importantly regulated by prior phosphorylation of serines 276 and 536.
- study provides the first example of a gene (SH#BGRL) that is downregulated in v-Rel-expressing cells that also plays a role in v-Rel transformation
- The expression of NF-kappaB p65 was related with tumor angiogenesis.
- The activation of p50 and p65 by tumor necrosis factor alpha suppresses the expression of the alpha1C subunit of Cav1.2 channels in human colonic circular smooth muscle cells
- In parathyroid tumors, p65 phosphorylation is dramatically increased.
- Data raise the possibility of a positive feedback loop in which NF-kappaB activation by oxidative stress leads to further radical production via NADPH oxidase subunit gp91(phox).
- NFkB has a role in VEGF signaling in endothelial cell survival
- The critical IRAK1 role in LMP1-induced NF-kappaB activation is in mediating p65/RelA S536 phosphorylation through an effect on p38 or other p65 S536 kinases.
- curcumin-mediated activation of JNK or induction of apoptosis does not require inhibition of p65
- These data support the significance of COMMD protein-protein interactions and provide new mechanistic insight into the function of this protein family in NF-kappaB signalling.
- NF-kappaB movement through the cytoplasm to the nucleus is independent of the cytoskeleton. NF-kappaB p65 is not associated with the dynein/dynactin molecular motor complex.
- NF-kappaB p65 directly interacted with the DNA-binding domain of RXRalpha and may prevent its binding to the consensus DNA sequences, thus inhibiting the transactivation by the PXR.RXRalpha complex.
- LRRC4 plays a major role in suppressing U251 cell proliferation by regulating the extracellular signal-regulated kinase (ERK)/Akt/NF-kappaBp65, STAT3, and JNK2/c-Jun pathways.
- results indicate that inflammatory signals regulate iodothyronine deiodinase type II expression predominantly via the nuclear factor-kappa B pathway in a direct transcriptional manner
- siRNA knockdown of p65 inhibits proteasome inhibitor-induced NF-kappaB transcriptional activity
- C/EBP beta association with NF-kappa B subunit p65/RelA blocks phosphorylation of p65, causing inhibition of NF-kappa B-mediated transcription in tumor necrosis factor (TNF)-tolerant cells.
- DEK functions to negatively regulate transcription of RelA/p65
- Results indicate that 14-3-3 proteins facilitate the nuclear export of IkappaBalpha-p65 complexes and are required for the appropriate regulation of NFkappaB signaling.
- findings show NFKB translocation is stimulated by the L. pneumophila virulence system & is required to support bacterial intracellular growth in macrophages
- Phosphorylation of ERK1/2 led to an activation of NFkB, and increased mRNA levels of the antioxidant enzyme manganese-superoxide dismutase (MnSOD).
- COX-2 induction by nickel compounds occurs via an IKKbeta/p65 NF-kappaB-dependent but IKKalpha- and p50-independent pathway and plays a crucial role in antagonizing nickel-induced cell apoptosis in Beas-2B cells
- CDDO and CDDO-Me directly block IKKbeta activity and thereby the NF-kappaB pathway by interacting with Cys-179 in the IKKbeta activation loop
- Novel interactions reveal a hitherto unknown function of IKKepsilon in the regulation of the alternative NF-kappaB activation pathway involving p52 and p65 are reported.
- These data implicate an important role of c-Src in phosphorylating RelA/p65 to promote the transcriptional activity of NF-kappaB and thereby ICAM-1 expression in endothelial cells.
- These data show that SIRT1 regulates cigarette smoke-mediated proinflammatory mediator release via NF-kappaB, implicating a role of SIRT1 in sustained inflammation and aging of the lungs.
- T lymphocytes from patients with active pulmonary tuberculosis (PTB) had significantly decreased expression of CD3zeta & absence of the p65/p50 heterodimer of NF- kappa B; findings provide a novel mechanism for the T cell dysfunction in patients with PTB
- Antigens CD3/CD28 activation induces the transactivation activity of both p65/RelA and c-Rel in T cells.
- Together, these studies reveal that phosphorylation of the SIMPL protein plays a critical role in SIMPL regulation by affecting both SIMPL subcellular localization and the p65 coactivator function of SIMPL.
- TNF-alpha enhances the binding of p65 to the promoter/enhancer regions of the MnSOD gene, which primes neuronal cells to develop resistance against subsequent exposure to beta-amyloid and FeSO(4).
- These data reveals for the first time that PDK1 and PKB may differentially activate NF-kappaB, and that TPCK may subserve a useful anti-inflammatory function by inhibiting IKKbeta.
- RelA/p65 associates with actin, accumulates in the nucleus, and induces ICAM-1 expression after thrombin stimulation of endothelial cells.
- Deficiency of RelA reduces cerebral infarct size in RelA transgenic mice.
- These results indicate that MYBBP1a is a novel NF-kappaB co-repressor of transcription that competes with p300 and may function to regulate cell type specific genes.
- the p38 MAPK/NF-kappaB/cyclin D1 signaling pathway might participate in the oncogenesis of extramammary Paget's disease
- Unequal alterations in the levels of activated NF-kappaB subunits p50 and p65 might provide insights into the mechanisms of NF-kappaB action and anti-TNF-alpha therapy in AS.
- two kappaB-binding sites were identified upstream from the start codon in the IL-20 gene
- Taken together, these results illustrate a role for p65 in regulating the ERVWE1 promoter and in TNFalpha-mediated induction of syncytin-1 in multiple sclerosis.
- Chlamydiae have the ability to interfere with the NF-kappaB pathway of host inflammatory response.
- These results indicate that the reactive oxygen species-mediated TNF-alpha-induced IL-8 transcription is regulated by NF-kappaB/RelA phosphorylation at the critical Ser(276) residue by PKAc, resulting in stable enhanceosome formation on target genes.
- The physical interaction between Daxx and p65 provides a functional framework for the inhibition of p65 acetylation by p300/CBP and subsequent repression of NF-kappaB transcriptional activity.
- These data suggest that nitric oxide as an inhibitor or activator of NF-kappaB p65 may depend on the state of activation of vascular endothelial cells in which it contacts.
- Data suggest that Twist-1 and -2 play an important role in NF-kappaB-dependent chemoresistance.
- Results indicate that antitumor and anti-inflammatory activities previously assigned to butein may be mediated in part through the direct inhibition of IKK, leading to the suppression of the NF-kappaB activation pathway.
- Inhibition of NFkappaB at G2-M diminished mitosis induced by constitutive activation of ERK5, providing a direct link between ERK5, NFkappaB, and regulation of G2-M progression.
- GRx-dependent S-glutathionylation of p65-NFkappaB is most likely responsible for NAC-mediated NFkappaB inactivation and enhanced hypoxic apoptosis
- Increased expression of NAD(P)H oxidase-p47phox and nuclear factor-kappaB p65 may contribute to endothelial oxidative stress with aging in humans.
- Frequent osteopontin expression is typical of, but not specific for malignant pleural mesothelioma, whereas it appears to select pulmonary adenocarcinoma cases with p65 and MMP-9 expression, suggesting a link with EGFR signalling pathways.
- These findings provide evidence for the involvement of the nuclear hormone receptors PPAR gamma and VDR in butyrate-mediated inhibition of inducible NF kappa B activation dependent on the stimulated signalling pathway.
- Review. In cells with mutant RelA lacking the nucleolar targeting domain treated with CDK4 inhibitor, RelA translocated from the cytoplasm to the nucleoplasm, but was excluded from the nucleolus. CDK4 inhibition did not induce apoptosis in these cells.
- increased apoptosis by dual knockdown of p65 and p50 may prove advantageous in preventing invasiveness and destructiveness of hyperplastic synoviocytes
- nuclear IKKalpha is required for p65 DNA binding in a gene-specific manner
- Pathophysiologically relevant homocysteine concentrations induce VCAM-1 expression through a prooxidant mechanism involving NF-kappaB.
- U2-OS cells were used to study direct interactions between fluorescent fusion proteins of ERalpha and the NF-kappaB subunits p50 and p65.
- calyculin A elicits phosphorylation of NF-kappaB on serine 536 in MG63 cells, resulting in the translocation of phospho-NF-kappaB to the nucleus, thereby promoting transcriptional activity of NF-kappaB-related genes
- High expression of RelA/p65 is correlated to an activation of the NF-kappaB pathway and indicates poor patient survival.
- Bortezomib reduced the levels of the p50 and p65 components of the canonical NF-kappaB pathway and reduced the level of p52 in the noncanonical NF-kappaB pathway, which is induced by EBV LMP1.
- The study demonstrates that CT441 is a tail-specific protease that is capable of interfering with the NF-kappaB pathway of host antimicrobial and inflammatory responses.
- Selective suppression of RELA in hepatitis virus-infected pregnant women manifesting severe liver damage and high mortality.
- These data support an unsuspected role for HLA-G in innate immunity by activating classical NF-kappaB pathway in natural killer cells.
- NF-kappaB recruits E2F1 to fully activate the transcription of NF-kappaB target genes.
- NOS2 regulates cytokine-induced S-nitrosylation of p65, resulting in decreased NF-kappaB binding to the NOS2 promoter, thereby inhibiting further NOS2 expression.
- In summary, pulse therapy resulted in a decreased level of activated p65 NF-kappaB subunits leading to decreased levels of transcriptionally active pro-inflammatory NF-kappaB.
- Activation of nuclear factor-kappa B p65 subunit is increased in peritoneal macrophages from patients with endometriosis.
- Results show that gankyrin directly binds to RelA.
- study reports that elevated (alpha6)beta4 integrin-dependent Rac-Pak1 signaling supports resistance to apoptosis in mammary acini by permitting stress-dependent activation of the p65 subunit of NF-kappaB through Pak1
- both IKKalpha and IKKbeta as well as NF-kappaB-inducing kinase are indispensable for lactoferrin-induced p65 phosphorylation
- Tumorigenic adenovirus type 12 E1A inhibits phosphorylation of NF-kappaB by PKAc, causing loss of DNA binding and transactivation.
- RelA was decreased in PBMC from patients with chronic pancreatitis.
- a novel regulatory role of p38 during neuroinflammation where this MAP kinase controls acetylation of NF-kappaB p65 by regulating acetyltransferase activity of coactivator p300.
- p65 induces transcriptional activation of several human & mouse hair keratin genes. It is co-expressed with HKs and may mediate the NF-kappaB pathway's activity. Binding sites for Ha5 were found.
- demonstrated that HCCs almost universally overexpress Bcl-3 and preferentially express nuclear p52 and p50, with little evidence of p65 activation
- findings identify RelA/NF-kappaB as a critical regulator of T-cell survival by affecting the balance of Bcl-2 family members.
- Our data suggest a crucial role of Ki-Ras:Akt1 complex in NF-kappaB transcriptional activation and enhancement of cell survival.
- Present immunofluorescence microscopy method to follow NF-kappaB nuclear translocation in primary human macrophages stimulated with LPS.
- ternary complex consisting of PPARdelta, p65/RelA, and HDAC1 in keratinocytes PPARdelta repression
- These results suggest that overexpression of p28(GANK) prevents the nuclear localization and inhibits the activity of NF-kappaB/RelA.
- RPS3 is an essential but previously unknown subunit of NF-kappaB involved in the regulation of key genes in rapid cellular activation responses.
- The proapoptotic effects of sulindac, sulindac sulfone and indomethacin are mediated by nucleolar translocation of the RelA(p65) subunit of NF-kappaB
- TNF-alpha stimulated tenascin-C expression through NF-kappaB signaling with RelA activation in cultured OA chondrocytes, suggesting involvement of tenascin-C in OA cartilage remodeling.
- High levels of TNFRI at the cell surface in patients with the C73R mutation hypersensitizes cells to stimulation by TNF, leading to increased NF-kappaB p65 subunit activation and an exaggerated proinflammatory response
- up-regulation of Smad7 by IL-1beta is mediated through the NF-kappaB pathway, especially the p65 subunit in chondrocytes
- analysis of a cross-talk between AP-1 and NF-kappaB
- the activation of NF-kappaB in human cancer cell lines and Min mice is inhibited by NO-donating aspirin
- AKIP1 colocalized with p65 within the cells and appeared to retain p65 in nucleus.
- Results show that nuclear p65/RelA expression was positively associated with tumour grade and T-category.
- phosphorylation of Ser-468 was indispensable for the physical interaction between RelA/p65 and GSK3beta.
- copine-I regulates the half-life of NF-kappaB transcriptional responses through a novel mechanism that involves endoproteolysis of the p65 protein
- RelA,was observed as increased expression in non-small cell lung cancer tissues
- p65 and p50 subunits of NF-kappaB can bind to alpha-actinin; the alpha-actinin-4 is important for the NF-kappaB nuclear translocation and its functions inside the nucleus.
- DNA binding of p50, Rel A, and c-Rel in primary CLL cells, and Rel A DNA binding was associated with in vitro survival, with high white cell count, and shorter lymphocyte doubling time
- RelA/p65 represses ARE-dependent gene transcription by depriving CBP from Nrf2 and facilitating recruitment of HDAC3 to MafK.
- Demonstration of a deregulation of the classical NF-kappaB rrelA pathway in ovarian cancer.
- Syk signals downstream of PKC-delta to mediate thrombin induced ICAM-1 expression in endothelial cells by increasing transcriptional capacity of NF-kappaB via a mechanism that relies on tyrosine phosphorylation of RelA/p65
- Promoter induction by RelA are controlled by a phosphorylation code influencing its interactions with coactivators and transcriptional elongation factors.
- These novel data demonstrate an IKK2-dependent, predominantly G-protein-independent pathway involved in PAR-2 regulation of NFkappaB phosphorylation in keratinocytes.
- the induction of inflammatory genes by farnesol is mediated by the activation of the NF-kappaB pathway and involves MEK1/2-ERK1/2-MSK1-dependent phosphorylation of p65/RelA(Ser(276))
- Cot was identified as a novel p65 interacting protein kinase.
- p50 and p65 subunits of NF-kappaB involved in the production of Wnt-1 by HepG2 cells
- These results provide insight into a glutamate-induced regulatory pathway distinct from that described for cytokine-induced NF-kappaB activation and have important implications with regard to both normal glial cell physiology and pathogenesis.
- RIG-1 - MAVS interacts with cytoplasmic 100-kDa NF-kappa B2 complexes via a novel retinoic acid-inducible gene-I - NF- kappa B-inducing kinase signaling pathway
- down-regulation of the NF-kappaB p65 subunit by RNA interference led to a reduction in cathepsin B expression in mitochondrial DNA-depleted osteosarcoma cells
- IL-8 and p53 protein expression is regulated through inverse activation of the p38 MAPK and the JNK pathways and the NF-kappaB p65 expression
- Results show that the p65 NF-kappaB host signaling pathway can differentially regulate influenza virus RNA synthesis.
- C/EBPbeta was found to have an important role in epithelial cell ICAM-1 regulation, while the adjacent NF-kappaB sequence binds the RelA/p65 and NF-kappaB1/p50 members of the NF-kappaB family to induce ICAM-1 expression in response to H. influenzae.
- protein kinase C betaII augments NF-kappaB-mediated TNF-alpha-induced transcription of the target gene CCL11, promoting p65 association with the CCL11 promoter, in human airway smooth muscle cells by phosphorylating p300/CBP-associated factor
- NF-kappaB p65 is activated in gastric carcinoma tissue, and is related to overall survival after chemotherapy.
- intraperitoneal administration of NF-kappaB p65 siRNA and paclitaxel may provide a breakthrough in the treatment of peritoneal metastasis of gastric cancer
- TGF-beta1 synergistically enhances TNF-alpha-induced NF-kappaB DNA binding activity via induction of RelA acetylation
- Hyperoxia combined with LPS induced a more prolonged duration of NF-kappaB activation.
- NFKB signal transduction is altered in premature rupture of fetal membranes
- tumor suppressor protein SMAR1 can modulate NF-kappaB transactivation and inhibit tumorigenesis by regulating NF-kappaB target genes
- expression of P-p65 is involved in NF-kappaB activation in diffuse large B-cell lymphoma
- thrombin-induced p65/RelA, AMPK, and PKCdelta activation were markedly reduced by knockdown of the TRPC isoform TRPC1 expressed in human endothelial cells and in endothelial cells obtained from Trpc4 knock-out mice.
- p27Kip1 is regulated by serine 276 phosphorylation of the p65 subunit of NF-kappaB
- effect of fhaB on the NFKB pathway in human monocytes, macrophages,epithelial cells; nuclear translocation of RelA, degradation of cytosolic IkappaB alpha, activation of the NF-kappaB pathway.
- These data suggest a mechanism for maintaining NF-kappaB activity in human T cells through the binding of the Caspase-3-generated carboxy-terminal fragment of p65/RelA to IkappaBalpha in order to protect wild-type p65/RelA from IkappaBalpha inhibition.
- Overexpression of P-AKT and NF-kappaB p65 were involved in the carcinogenesis and metastasis of ovarian cancer.
- Brd4 as a novel coactivator of NF-kappaB through specifically binding to acetylated lysine-310 of RelA.
- Rel A is an independent prognostic marker of survival in CLL and seems to have the unique capacity to predict the duration of response to therapy.
- plays a crucial role in BMP-2 expression and acetylation of NF-kappaB p65 and p50 subunits by TSA treatment may activate the BMP-2 promoter.
- This study provides therefore a direct link between MSK1-mediated phosphorylation of Ser276 p65 of NF-kappaB, allowing its binding to the SCF intronic enhancer, and pathophysiological SCF expression in inflammation.