BCL3

BCL3

A gene on 19q13.1-q13.2, which encodes a protein that functions as a transcriptional co-activator which acts by associating with NF-kappa B homodimers. BCL3’s protein product contains 7 ankyrin repeats similar to those found in I kappa B; BCL3 may interfere with binding of 50-kD subunit of NF kappa B to DNA.
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Among the dysregulated 516 genes in the MI model group, 12 were transcription factors, including CEBPD, CREB3, BCL3, SIX4, NFATC4, MAFF, ERF, NFIB, MITF, AEBP1, EGR2, and PRRX2.
It shows that TFs such as BCL11A, BCL3, EBF, EBF1, ERa, ERRA, FOXA1/2, HNF4A, HNF4G, IRF4, MAfF, NANOG, POU5F1, PU1, SETDB1, STAT2/3, and ZNF274 were significantly hypermethylated in the OST-7D group compared with those in the OST-0D group, and TFs including AP-2[alpha], BAF170, c-Fos, c-JUN, CEBPB, GATA2, GATA3, GR, MAfF, NF[kappa]B, P300, SIRT6, TAL1, and TCF4 were significantly hypomethylated in the OST-7D group compared with those in the OST-0D group (Supplementary Figure 1).
In a mouse model, the transcriptional coregulator B cell leukemia/lymphoma 3 (Bcl3) was identified to downregulate emergency granulopoiesis as consequence of a transplant-mediated ischemia/reperfusion lung injury, limiting pulmonary damage [152].
High expression of BCL3 in human myeloma cells is associated with increased proliferation and inferior prognosis.
These genes encoded cytokines (CSF3, CSF2, CCL3, TNF, CCR1, IL13, KIT, CCL5, CCL4, IL10, CXCL10, IL12RB2, IFNG, IL1B, IL1A, IL8, MET, CD40, HGF, LEP, CXCL16, CX3CR1, CCR2, PDGFRA, IL12B, IL2), lipid metabolism related genes (CD36, GPX4, LPIN1, LPL, LPB), transcription regulators (BCL3, FOS and NFKBIA), receptors (TNF, IL8, RELA, TLR1, TIRAP, TLR2, NFKBIA, NFKB1, TLR4, CD40, CCL5, CXCL10, FOS, JUN, MAP3K8, IL1B, LBP, IL12B, CD14, SPP1), and others such as SELP, SELL, and SOD1, all play a role in some aspect of the immune response including cytokine activity (IL10, TNF, IL8, and IL1B), cell adhesion (SELL and SELP), immune activation (CD14 and TLR2), acute phase reaction (TNF, IL1B, and SAA3), apoptosis (BCL2, BAX).
In addition, the chemical incompatibility of the BCl3 y BBr3 boron sources that, under the reaction conditions, can react as halogenating reagents of the benzenic ring in the phthalonitrile precursors has to be taken into account if a better synthetic protocol is going to be developed.
At the same time, binase promoted increased expression of inhibitors of this pathway, including NF[kappa]BIA (I[kappa]-B protein which inactivates NF-[kappa]B by trapping it in the cytoplasm) as well as NF[kappa]BIZ and BCL3 [21], indicative for the activation of counteracting pathways in cells that would lead to signal commotion with the result of cell death.
In addition, genes located at the 19q13 are the BAX and BCL3 apoptosis related genes [39], genes involved in cell cycle progression that codify for cyclins, such as CCNE1, and genes codifying for transcription factors, such as FOSB [40], among others [41].
This affects the innate response, leading to autoimmunity characterized by autoantibody formation by B cells, complement activation, and Bcl3 depletion, which inhibits granulopoiesis production [10, 11, 22, 97, 152, 177-180].
TOKYO, Feb 4, 2016 - (JCN Newswire) - Showa Denko (SDK) (TOKYO: 4004) has decided to increase its capacity to produce high-purity boron trichloride (BCl3), which is a kind of specialty gas used in the manufacture of electronic materials, to 1.5 times of the previous level.
Moreover, downregulated BCL3, which participates in the TNF pathway in the adipose tissue of the bladder wall, leads to reduced inflammation in bladder carcinogenesis [35].