Early growth response-1-dependent apoptosis is mediated by p53

The early growth response-1 (EGR-1) protein is an anti-proliferative signal for certain tumor cells and is required for apoptosis induced by stimuli that elevate intracellular Ca2+. We present evidence that EGR-1 transactivates the promoter of the p53 gene and up-regulates p53 RNA and protein levels. Inhibition of p53 function with dominant-negative p53 mutants abrogates EGR-1-dependent apoptosis. These findings establish a direct functional link between EGR-1 and the p53-mediated cell death pathway and suggest that mutant forms of p53 in tumor cells may provide resistance to the anti-proliferative effects of EGR-1.     

Activation of syk in an immature B cell line does not require lyn activity

BKS-2 is an immature B cell lymphoma that undergoes apoptotic cell death when signaled via its surface IgM receptor. To study the signaling components of surface IgM mediated apoptosis in B lymphoma cells, we generated mutants of BKS-2 that were resistant to anti-IgM induced apoptosis. One mutant cell line, 1.B5, did not undergo apoptotic cell death upon treatment with anti-IgM antibodies and also did not exhibit elevation of intracellular Ca2+ in response to cross-linking of surface IgM. This appeared to be due to a defect in protein tyrosine kinase (PTK) activity since fewer proteins were tyrosine phosphorylated in the mutant cells stimulated with anti-IgM when compared to wild type BKS-2. Subsequently, we showed that protein tyrosine kinases lyn and blk were inducibly tyrosine phosphorylated in the wild type BKS-2 but not in 1.B5 mutant cells in response to anti-IgM. Also the kinase activity of lyn was elevated in the wild type but not in mutant cells upon triggering through surface IgM. Furthermore, tyrosine phosphorylation of CD19, a known substrate of lyn, was inducible in anti-IgM stimulated BKS-2 cells but severely reduced in 1.B5 cells. In contrast, kinase activity of another src kinase, blk, was increased on anti-IgM stimulation in both wild type and mutant cells. Surprisingly, syk, a non-src protein tyrosine kinase important for surface IgM mediated signaling, was tyrosine phosphorylated in the lyn deficient mutant cells as well as in the wild type BKS-2 cells. Furthermore, anti-IgM induced increase in kinase activity of syk was similar in the mutant and wild type cells. Thus, in contrast to other studies that propose syk to be a downstream target of src family kinases, syk may act upstream of lyn in immature B cells. Consistent with a functional syk, its target, phospholipase gamma2 (PLC-gamma2) was normally tyrosine phosphorylated in mutant cells.     

Enhancing cooperative spectrum sensing in cognitive radio ad hoc networks using priority-based two-stage detection model

Cooperation among unlicensed secondary users was more significant in cognitive radio ad hoc networks (CRAHNs). The main challenges of CRAHNs now a day address the main issues of spectrum scarcity and underutilization. Due to the lack of channel sensing, cooperative spectrum sensing (CSS) is the main challenge in CRAHNs. Efficient CSS is more essential to enhance the detection of performance by utilizing the theoretical studies of spatially distributed secondary users (SUs). This paper uses the priority-based two-stage detection model (PBTSDM) to analyze the cooperation strategy among secondary users (SUs) and primary users (PUs). SUs in distributed CSS sense continuously amongst themselves and take unified decision on the presence or absence of PUs by using entropy-based energy detection mechanism. The simulation results reveal that the sensing accuracy in terms of sensing time and energy efficiency (in terms of minimum energy consumption) increased significantly by using the proposed scheme.