Results 201 to 210 of about 1,855,106 (245)
Childhood brain tumours instruct cranial haematopoiesis and immunotolerance
Cooper E +26 more
europepmc +1 more source
The opposite effects of stringent response on phage infection of <i>Pseudomonas putida</i>. [PDF]
Lewańczyk AC +5 more
europepmc +1 more source
Therapeutic targeting of FOSL1 and RELA-dependent transcriptional mechanisms to suppress pancreatic cancer metastasis. [PDF]
Aggrey-Fynn JE +8 more
europepmc +1 more source
Loss of <i>Trp53</i> results in a hypoactive T cell phenotype accompanied by reduced pro-inflammatory signaling in a syngeneic orthotopic mouse model of ovarian high-grade serous carcinoma. [PDF]
Haagsma J +6 more
europepmc +1 more source
NF-κB RelA Phosphorylation Regulates RelA Acetylation [PDF]
The nuclear functions of NF-kappaB p50/RelA heterodimers are regulated in part by posttranslational modifications of its RelA subunit, including phosphorylation and acetylation. Acetylation at lysines 218, 221, and 310 differentially regulates RelA's DNA binding activity, assembly with IkappaBalpha, and transcriptional activity.
Lin-Feng Chen +2 more
exaly +3 more sources
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Biochemistry, 2004
Nuclear factor-kappaB (NF-kappaB) transcription factors are important in regulating the immune response and play critical roles in the pathogenesis of chronic inflammatory diseases and a variety of human cancers. Agents that target specific NF-kappaB dimers may serve as therapeutic agents for the prevention of pathogenic immune responses.
Suzanne E, Bassett +8 more
openaire +2 more sources
Nuclear factor-kappaB (NF-kappaB) transcription factors are important in regulating the immune response and play critical roles in the pathogenesis of chronic inflammatory diseases and a variety of human cancers. Agents that target specific NF-kappaB dimers may serve as therapeutic agents for the prevention of pathogenic immune responses.
Suzanne E, Bassett +8 more
openaire +2 more sources
Nonsense and insertion mutants in the relA gene of E. coli: Cloning relA
Cell, 1978We have made use of lysogens of a specialized transducing bacteriophage, lambdapyrG+ relA+, to select nonsense (relAnon) and insertion (relAins) mutations in the relA gene. Three independent relAnon mutants were isolated on the phage. In all three, the relaxed phenotype was suppressed by supD, supE, supF or sup6.
J D, Friesen, G, An, N P, Fiil
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Regulation of the RelA (p65) transactivation domain
Biochemical Society Transactions, 2008The RelA (p65) NF-κB (nuclear factor κB) subunit contains an extremely active C-terminal transcriptional activation domain, required for its cellular function. In the present article, we review our knowledge of this domain, its modifications and its known interacting proteins.
O'Shea, John M., Perkins, Neil D.
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ChemInform Abstract: BENZALPHTHALIMIDINES AND RELA
Chemischer Informationsdienst, 1978AbstractDas Chlorphthalsäureanhydrid (I) reagiert mit der Essigsäure (II) zu den isomeren Chlorbenzalphthaliden (IIIa) und (IIIb), die jeweils in Gegenwart von Alkali zu dem Indandion (IV) isomerisieren.
A. M. ISLAM +2 more
openaire +1 more source
Journal of Cellular Physiology, 2018
AbstractPancreatic ductal adenocarcinoma (PDAC) remains a challenging malignancy due to distant metastasis. RELA, a major component of the NF‐κB pathway, could serve as an oncogene through activating proliferation or migration‐related gene expression, including NEAT1, a well‐known oncogenic long noncoding RNA.
Zhen Luo +7 more
openaire +2 more sources
AbstractPancreatic ductal adenocarcinoma (PDAC) remains a challenging malignancy due to distant metastasis. RELA, a major component of the NF‐κB pathway, could serve as an oncogene through activating proliferation or migration‐related gene expression, including NEAT1, a well‐known oncogenic long noncoding RNA.
Zhen Luo +7 more
openaire +2 more sources

