Mechanisms Of Ebv Latent Membrane Protein Trafficking Essay

Social withdrawal is a core negative symptom in schizophrenia. It is well documented that individuals with schizophrenia have difficulty in making and keeping social relationships, in coping with social situations, and in social communication. Such impairment may result in insubstantial functional disability and in the quality of life. However, the neurobiology underlying this core symptom is not well understood, and the current medications failed to provide efficiency treatment. The ErbB pathway has been genetically and functionally implicated in schizophrenia, and in developing and regulating complex behaviors. Numerous findings support the dysregulation of the ErbB signaling in complex behaviors as learning and memory, reward seeking and

This virus brings about a lost lasting infection that affects the general nervous system of various individuals after they have acquired the infection for the first time. It is normally latent in nature, but various nonspecific or unexpected inflammations cause some reactivation for example herpes labialis (Mawanda & Wallace, 2013 pp.161). Some scientific studies have shown that HSV-1 can easily enter or penetrate human body by the help of various routes and can consequently repeatedly occur in absence of neurological signs. Studies have also indicated that HSV-1 greatly and latently infects the nervous system of humans. This virus group of HSV-1 was greatly associated with the different risk factors for the occurrence of dementia and consequently most researchers have found out that there is a great positive significant relationship between HSV-1 and Alzheimer’s disease.

By utilizing these two transgene expressions in a synchronized way, the adenovirus is granted the ability to replicate, specifically when it is within a tumor cell. The promoter hTERT controls the specificity of E1a’s ability for viral replication. This assures that the adenovirus only replicates within cancer cells because the gene marker is only triggered where the hTERT expression is prevalent, which, as indicated earlier, is only within cancerous cells.

Translocation Brings the MYC oncogene located at 8q24 into juxtaposition with –the transcriptionally active-immunoglobulin heavy chain IGH genes at locus 14q32 or the light chain loci [ ĸ (t(2;8)(p12;q24) or ʎ t(8;22)(q24;q11)] leading to its ectopic expression and hence, driving the uncontrolled proliferation of BL cells. Though believed to be critical for BL tumorigenesis, studies revealed that Myc translocation –solely- is not sufficient to fully transform B-cells to BL. In fact, other secondary oncogenic mechanisms seem to be as essential in the process of lymphomagenesis (5) (6). Table(2) summarizes genetic aberrations frequently reported in BLs and claimed to play a role in oncogenic transformation of

These viruses have a 145 to 150 kb genomic DNA and glycoproteins that are important for cell attachment, entry and cell-to-cell spreading and induction of immune responses [3,4]. The common characteristics between all herpesvirus infections are latency

Nasopharyngeal carcinoma (NPC) is a rare head and neck cancer, although in Asian individuals of southern Chinese descent observed high incidence of NPC (Lo et al., 2004). The pathogenesis of NPC is multifactorial connecting with viral, genetic and environmental factors. The Epstein-Barr virus (EBV) with nonkeratinizing NPC in Asian populations has been well documented in 1970s (Shanmugaratnam and Sobin, 1991), however, it is not clearly associated with non-Asian patients (Raab and Epstein, 2002; Lo et al., 2004). Inactive EBV infection is found in NPC and high-grade dysplasia, however is not obviously present in the normal nasopharyngeal epithelium (Raab and Epstein, 2002). Previous studies show unclear

Presenilins have 9 transmembrane domains are evolutionarily conserved integral membrane proteins. Presenilin, along with Aph-1, Pen-2 and nicastrin constitute integral components of a multi-protein protease complex, termed γ-secretase, which is responsible for the intramembranous cleavage of both the amyloid precursor protein (APP) and Notch. Many γ-secretase substrates have diverse cellular functions, including cell adhesion, ion conductance, and receptor kinase activity, to name a few. Presenilins are also known to exert γ-secretase-independent activities including regulation of the Wnt/β-catenin signalling pathway, calcium release from the ER, and lysosomal proteolysis. PS1 operates as a negative regulator of the Wnt/β-catenin signaling

The early viral genes E6 and E7 can influence both replication and transcription of the virus, and also interacts with host regulatory proteins [2]. Upon infection of the host, the viral genome ring is disrupted leading to its ability to incorporate its genome into that of the host's [2]. Once the viral early proteins interact with the host’s regulatory proteins, the host cells will lose function of regulating tumor suppression, ultimately stimulating the proliferation of the HPV infected cells [2][7]. Papillomaviruses tend to replicate within cells through the lysogenic pathway, and incorporate its viral genome into the host’s genome [7]. Stated earlier, early detection of this particular virus is challenging because the

Importantly, the ERM protein ezrin itself is a well-known mediator of metastasis (Elliott et al., 2005; Khanna et al., 2004; Meng et al., 2010). Many clinical studies have linked high expression of ezrin with poor outcome in cancer patients suffering from a wide variety of cancers, including prostate, breast can lung cancer (Clucas and Valderrama, 2014). Interestingly, specifically the abnormal distribution of ezrin in breast cancer patients, from the apical regions of non-tumorigenic cells to motile projections in invasive cells, has been correlated with poor prognosis (Sarrio et al., 2006). In addition, it has previously been indicated as an important regulator of metastasis in the murine carcinoma cell line AC2M2 (Elliott et al., 2005). Furthermore, ezrin overexpression has been shown in various studies to promote the survival, migration and/or invasion of cancer cells into surrounding tissue and to disrupt cell-cell contacts (Clucas and Valderrama, 2014).

Experiments and extensive screenings have shown that mutations in FBXW7 are found in approximately 6% of all primary human cancer. T cell acute lymphoblastic leukaemia was the cancer in which exhibited the most frequent mutation of FBXW7. Mouse models have been utilized to further understand the physiological functions of FBXW7 in tumorigenesis. These mice that did not express FBXW7 were analysed and studied especially in the areas of their bone marrow and intestines. Mice with FBXW7 completely knocked out exhibited thymic lymphoma due to the excessive collection of MYC. Biochemical evidence also insinuates that FBXW7 exerts its tumour-suppressant function through the promotion of degradation of various oncoproteins (proteins that promote cancer growth). FBXO11, on the other hand, has shown to target the BCL-6 oncoprotein for ubiquitylation and the following degradation. The overexpression of FBXO11 stopped and inhibited the growth of the cell and induced apoptosis (cell death) by promoting the BCL-6 degradation in large B cell

Local invasion represents the first step of the metastatic cascade and requires profound changes in cell-cell adhesion, cell-ECM interactions, proteolysis of ECM components and acquisition of migratory properties. Cancer cells can deploy different types of cell migration, including collective migration and single cell migration50. Predominantly, most epithelial cancer cells use collective cell migration, however some cancer cells may co-opt the biological program known as the EMT to migrate as single cells. EMT is a critical process for multiple aspects of normal embryonic development51. Since its discovery, there has been the realization that there are many parallels in the mechanisms that govern EMT in embryonic development and in cancer

The gammaherpesviruses Epstein-Barr virus (EBV) and Kaposi’s sarcoma herpesvirus (KSHV) establish lifelong persistent infection in the host and are capable of causing several lymphomas and neoplasms. Gammaherpesviruses have two distinct phases in the life cycle: lytic replication and latency. Lytic replication is cleared by the immune system, the virus evades detection by the immune system and maintains a lifelong persistence in the host by establishing latency. Viral latency in B cells is the critical event associated with tumorgenesis. The innate immune system employs the Type I Interferon (IFN) response to combat viral infection. IFN family of cytokines signals the presence of an intracellular infection and activates the transcription of IFN stimulated genes (ISGs). ISG products are a diverse collection of proteins that promote antiviral and immunomodulatory functions. This proposal

Intrinsic immunity uses cell-based responses with antiviral properties, and is frequently expressed at a constitutive level [24]. For example, promyelocytic leukemia nuclear bodies (PML-NBs), which are sub-nuclear structures, possess antiviral effects against both DNA and RNA viruses [36]. BKV is hypothesised to resist these antiviral effects by reforming PML-NBs and causing the dispersion of two major protein components, Daxx and SP100 [36].

This increased the importance of unraveling the underlying molecular events associated with CSC population, as they could serve as early detectors of malignant potential in OED and prognosis of OSCC. Thus, the signaling pathways required for the maintenance of CSCs became candidate targets of recent investigations in this field. Currently, light was shed on B-lymphoma Moloney murine leukemia virus insertion region-1 (BMI-1) which has been implicated in the regulation of CSCs.

Exosomes are membranous vesicles enclosed in lipid bilayers with diameter of 30-100nm and are responsible in carrying cytoplasmic proteins such as Rab proteins and actin-binding proteins and signal transduction molecules such as G-proteins and protein kinases, as well as some heat-shock proteins like Hsp70 and tetraspanins like CD9 [5-30]. Exosomal proteins can directly represent the specific profiles of their cells of origin, for