BCL2


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BCL2

(bē′sē-ĕl-tōō′)
n.
A gene associated with non-Hodgkin's lymphoma that normally helps regulate the life span of a white blood cell but when mutated prevents such cells from dying, allowing possible further mutations and the development of cancer.
The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.
References in periodicals archive ?
This study determined the mRNA expression levels of the pro-apoptotic BAX, anti-apoptotic BCL2 as well as the anti-angiogenic VEGF splice variant VEGF165b after a 120 h treatment with lopinavir and curcumin (individually and in combination) in HCS-2 and NCE16IIA cervical cell lines.
The presence of an IGH-BCL2 rearrangement was confirmed by FISH analysis in at least 1 sample from each patient, including the 2 cases with insertion of BCL2 into the IGH locus.
BCL2 genotypes at the promoter region (-938) SNP were evaluated by restriction fragment length polymorphism polymerase chain reaction technique (RFLP- PCR).
Analisis inmunohistoquimico Despues de la coloracion inmunohistoquimica se observo que 13 muestras (45%) presentaban el 0% de celulas coloreadas con el marcador BCL2, 6 muestras (21%) presentaban el 25% de las celulas coloreadas, 6 muestras (21%) presentaban el 50% las celulas coloreadas y 4 muestras (14%) presentaban el 75% de las celulas coloreadas, y ninguna muestra tenia un 100% de celulas coloreadas para el marcador en estudio.
Considering the increase of the BCL2 gene expression during the MOLT-4 cells co-cultured with MSCs under the hypoxic condition, the apoptosis lowering was expectable.
Present study is based on the genotyping of BCL2 SNP in Pakistani population and screening of specific targeted inhibitors that binds at increased BH3 sites in cells due to increased expression of BCL2 protein in cell and decrease the anticancer drugs resistance in acute lymphoblastic leukemia (ALL) patients.
Genes AKT1, BAD, BAX, BCL2, CASP3, CASP8, CASP9, MYC, PIK3CD, MAPK1, MAPK10, and CYCS are commonly expressed in the cluster of colorectal cancer, neuronal signaling pathway, neuronal death, amytrophic lateral aclerosis, and tuberculosis [51].
Our previous results show that PPAR[alpha] induces the antiapoptotic Bcl2 protein ubiquitination and degradation [6].
Bcl2, Ccnd1, Cdk6, and Sox4), intestinal stem cells (Lgr5, Olfm4, and Bmi1) [10], mucin biology (Muc2 and Muc6), and tight junctions (occludin, zonulin-1, and Jam) was analyzed using real-time PCR (Table S1).
Immunohistochemical staining was positive for CD34, bcl2 (Figure 3), and vimentin (Figure 4) but was negative for cytokeratin, SMA, desmin, and S100.
The relative mRNA expression levels of T-bet, GATA3, PU.1, RORc, AHR, Foxp3, Bcl2, Bax, and a-SMA were measured, and the results were normalized against the expression levels of GAPDH.
Immunohistochemistry reactions were performed using antibodies against Ki67 (Dako, Glostrup, Denmark; clone MIB-1, DAKO 7240, dilution 1:200); BrdU (Neomarkers, Fremont, CA, USA; clone Bu20a,1848-P, dilution 1:1000); BCL2 (Dako M0887, clone 124, dilution 1:500); [p27.sup.Kip1] (Dako M7203, clone Sx53G8, dilution 1:1000); Vitamin D receptor (Millipore, Temecula, CA, USA; clone 9A7, Millipore 04-1526, dilution 1:30), followed by detection through Lab Vision[TM] UltraVision[TM] LP Detection System: HRP Polymer/DAB Plus Chromogen (visualized using 3.3'diaminobenzedine tetrahydrochloride (DAB, D-5637, Sigma, St.