Displaying publications 1 - 20 of 193 in total

Abstract:
Sort:
  1. The linkage between microRNA and cancer and its delivery as cancer therapy: A mini-review
    Syed Najmuddin SUF, Kamarudin AA, Abdul Sani S, Norrrahim MNF, Abdul Latif N', Wah LGP
    Cell Mol Biol (Noisy-le-grand), 2023 Jul 31;69(7):7-18.
    PMID: 37715444 DOI: 10.14715/cmb/2023.69.7.2
    The central dogma of molecular biology was no longer "central" after ground-breaking discoveries conveyed gene expression involves more complex physiological functions in cancer pathogenesis over the last decade. MicroRNAs (miRNAs) are short non-coding RNA that regulate gene expression, affecting key molecular pathways involved in sustaining the proliferative signalling for tumour development, evasion of cellular death, invasion, angiogenesis, as well as metastasis in a plethora of cancer types. MiRNA expression is dysregulated in human cancer through a number of processes, including miRNA gene amplification or deletion, faulty miRNA transcriptional regulation, dysregulated epigenetic alterations, and flaws in the miRNA biogenesis machinery. As a result, the current progress of treatment intervention focuses on modifying the miRNA levels in cancer therapeutics. Nevertheless, the mode of delivery and current management of miRNA therapies remains one of the many questions that need to be addressed. Here, we provided a comprehensive mini-review outlining the role of miRNA in cancer as well as its mode of delivery which includes liposomes, viral vectors, inorganic material-based nanoparticles, and cell-derived membrane vesicles. Likewise, the regulation of miRNA in other diseases and their challenges in translational research was also thoroughly discussed.
    Matched MeSH terms: Cell Death
  2. Fulltext SARS CoV-2 aggravates cellular metabolism mediated complications in COVID-19 infection
    Singh Y, Gupta G, Kazmi I, Al-Abbasi FA, Negi P, Chellappan DK, et al.
    Dermatol Ther, 2020 11;33(6):e13871.
    PMID: 32558055 DOI: 10.1111/dth.13871
    Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the primary causative organism in corona virus disease-19 (COVID-19) infections, is a novel member of the human coronavirus family which was first identified in Wuhan, China, towards the end of 2019. This letter reveals new vital missing links in our current understanding of the mechanisms that lead to cell death triggered by ferroptotic stress in COVID-19 infection. It further reveal the importance of homocysteine mediated trans-sulfuration pathway in COVID-19 infection. Hence, Vitamin B6, folic acid, and Vitamin B12 should be incorporated in the treatment regimen for SARS CoV-2 infections to suppress complications, as the virus mediates altered host cell metabolism.
    Matched MeSH terms: Cell Death/physiology*
  3. Fulltext Involvement of the uridine cytidine kinase 2 enzyme in cancer cell death: A molecular crosstalk between the enzyme and cellular apoptosis induction
    Malami I, Abdul AB
    Biomed Pharmacother, 2019 Jan;109:1506-1510.
    PMID: 30551402 DOI: 10.1016/j.biopha.2018.10.200
    Apoptosis is a series of molecular signalling regulating normal cellular growth and development. Cells resistance to apoptosis, however, leads to uncontrolled proliferation. Research involving cancer cell death is one of the most important targeted areas in the discovery of novel anticancer therapy. There are several biochemical pathways that are liked towards cancer cell death of which, uridine-cytidine kinase 2 (UCK2) was recently linked to cell apoptosis induction. UCK2 is responsible for the phosphorylation of uridine and cytidine to their corresponding monophosphate in a salvage pathway of pyrimidine nucleotides biosynthesis. Cytotoxic ribonucleoside analogues that target UCK2 enzyme activity are currently being investigated in clinical trials useful for cancer treatment. Whilst findings have clearly shown that these antimetabolites inhibit cancer development in clinical settings, they have yet to establish linking cytotoxic nucleoside analogues to cancer cell death. In this present review, we propose the probable molecular crosstalk involving UCK2 protein and cancer cell death through cell cycle arrest and triggering of apoptosis involving proteins, MDM2 and the subsequent activation of p53.
    Matched MeSH terms: Cell Death/physiology*
  4. Proteomic analysis of flavokawain C-induced cell death in HCT 116 colon carcinoma cell line
    Phang CW, Gandah NA, Abd Malek SN, Karsani SA
    Eur J Pharmacol, 2019 Jun 15;853:388-399.
    PMID: 31014923 DOI: 10.1016/j.ejphar.2019.04.032
    Flavokawain C (FKC), a naturally occurring chalcone, has previously been shown to inhibit the growth of colon carcinoma HCT 116 cells through induction of apoptosis and cell cycle arrest. However, the possible underlying mechanisms of cell death as a response to FKC treatment remains unclear. In this study, we performed proteomic analysis of HCT 116 cells treated with FKC to identify proteins that change in abundance. This was followed by bioinformatic analysis to predict possible associated molecular targets or pathways involved in the observed effects of FKC. A total of 35 proteins that changed in abundance (17 increased and 18 decreased) were identified through two-dimensional gel electrophoresis followed by matrix-assisted laser desorption ionisation time-of-flight mass spectrometry (MALDI-TOF/TOF MS). Using the Ingenuity Pathway Analysis (IPA), these proteins were predicted to be involved in cell death and survival, cell cycle, cellular growth and proliferation, protein synthesis, post-translational modification and amino acid metabolism by. Further analysis of the transcript levels of selected proteins using qPCR showed that some of the genes exhibited similar change of profile to that of the proteins'. Our results have provided novel insights into the potential molecular mechanisms underlying FKC-induced apoptosis or cell death in colon cancer cells.
    Matched MeSH terms: Cell Death/drug effects
  5. Susceptibility to drug-induced haemolysis in Singapore
    VELLA F
    Med J Malaya, 1959 Jun;13:298-308.
    PMID: 13841622
    Matched MeSH terms: Cell Death*
  6. Cytotoxicity and electron microscopy of cell death induced by goniothalamin
    Ali AM, Mackeen MM, Hamid M, Aun QB, Zauyah Y, Azimahtol HL, et al.
    Planta Med, 1997 Feb;63(1):81-3.
    PMID: 9063100
    The cytotoxicity of goniothalamin was found to be strong towards both cancerous (HGC-27, MCF-7, PANC-1, HeLa), and non-cancerous (3T3) cell lines, especially in cases of dividing cells. Drug exposure studies indicated that the cytotoxic action of goniothalamin was time- and dose-dependent. At the ultrastructural level, goniothalamin-induced cytotoxicity revealed a necrotic mode of cell death towards MCF-7 cells.
    Matched MeSH terms: Cell Death/drug effects*
  7. Isolation and structural modifications of ananixanthone from Calophyllum teysmannii and their cytotoxic activities
    Kar Wei L, Zamakshshari NH, Ee GCL, Mah SH, Mohd Nor SM
    Nat Prod Res, 2018 Sep;32(18):2147-2151.
    PMID: 28826239 DOI: 10.1080/14786419.2017.1367781
    Two naturally occurring xanthones, ananixanthone (1) and β-mangostin (2), were isolated using column chromatographic method from the n-hexane and methanol extracts of Calophyllum teysmannii, respectively. The major constituent, ananixanthone (1), was subjected to structural modifications via acetylation, methylation and benzylation yielding four new xanthone derivatives, ananixanthone monoacetate (3), ananixanthone diacetate (4), 5-methoxyananixanthone (5) and 5-O-benzylananixanthone (6). Compound 1 together with its four new derivatives were subjected to MTT assay against three cancer cell lines; SNU-1, K562 and LS174T. The results indicated that the parent compound has greater cytotoxicity capabilities against SNU-1 and K562 cell lines with IC50 values of 8.97 ± 0.11 and 2.96 ± 0.06 μg/mL, respectively. Compound 5 on the other hand exhibited better cytotoxicity against LS174T cell line with an IC50 value of 5.76 ± 1.07 μg/mL.
    Matched MeSH terms: Cell Death/drug effects
  8. Fulltext Phylattrin, a new cytotoxic xanthone from Calophyllum soulattri
    Mah SH, Ee GC, Teh SS, Rahmani M, Lim YM, Go R
    Molecules, 2012 Jul 10;17(7):8303-11.
    PMID: 22781442 DOI: 10.3390/molecules17078303
    Our continuing studies on secondary metabolites from the stem bark of Calophyllum soulattri has led to the isolation of another new diprenylated xanthone, phylattrin (1), in addition to five other xanthones and two common sterols. The xanthones are soulattrin (2), caloxanthone C (3), macluraxanthone (4), brasixanthone B (5) and trapezifolixanthone (6) while the sterols are stigmasterol (7) and β-sitosterol (8). The structures of these compounds were determined on the basis of spectroscopic analyses such as 1D and 2D-NMR, HRESIMS, IR and UV. Compounds 1-7 exhibited moderate cytotoxic activities against SNU-1, HeLa, Hep G2, NCI-H23, K562, Raji, LS174T, IMR-32 and SK-MEL-28 cells.
    Matched MeSH terms: Cell Death/drug effects
  9. Fulltext Acquired radioresistance in EMT6 mouse mammary carcinoma cell line is mediated by CTLA-4 and PD-1 through JAK/STAT/PI3K pathway
    Sham NFR, Hasani NAH, Hasan N, Karim MKA, Fuad SBSA, Hasbullah HH, et al.
    Sci Rep, 2023 Feb 22;13(1):3108.
    PMID: 36813833 DOI: 10.1038/s41598-023-29925-x
    Cancer recurrence is often associated with the acquisition of radioresistance by cancer tissues due to failure in radiotherapy. The underlying mechanism leading to the development of acquired radioresistance in the EMT6 mouse mammary carcinoma cell line and the potential pathway involved was investigated by comparing differential gene expressions between parental and acquired radioresistance cells. EMT6 cell line was exposed to 2 Gy/per cycle of gamma-ray and the survival fraction between EMT6-treated and parental cells was compared. EMT6RR_MJI (acquired radioresistance) cells was developed after 8 cycles of fractionated irradiation. The development of EMT6RR_MJI cells was confirmed with further irradiation at different doses of gamma-ray, and both the survival fraction and migration rates were measured. Higher survival fraction and migration rates were obtained in EMT6RR_MJI cells after exposure to 4 Gy and 8 Gy gamma-ray irradiations compared to their parental cells. Gene expression between EMT6RR_MJI and parental cells was compared, and 16 genes identified to possess more than tenfold changes were selected and validated using RT-PCR. Out of these genes, 5 were significantly up-regulated i.e., IL-6, PDL-1, AXL, GAS6 and APCDD1. Based on pathway analysis software, the development of acquired radioresistance in EMT6RR_MJI was hypothesized through JAK/STAT/PI3K pathway. Presently, CTLA-4 and PD-1 were determined to be associated with JAK/STAT/PI3K pathway, where both their expressions were significantly increased in EMT6RR_MJI compared to parental cells in the 1st, 4th and 8th cycle of radiation. As a conclusion, the current findings provided a mechanistic platform for the development of acquired radioresistance in EMT6RR_MJI through overexpression of CTLA-4 and PD-1, and novel knowledge on therapeutic targets for recurrent radioresistant cancers.
    Matched MeSH terms: Programmed Cell Death 1 Receptor*
  10. IL-8 and PI3K pathway influence the susceptibility of TRAIL-sensitive colorectal cancer cells to TRAIL-induced cell death
    Jong KXJ, Mohamed EHM, Syafruddin SE, Faruqu FN, Vellasamy KM, Ibrahim K, et al.
    Mol Biol Rep, 2024 Sep 13;51(1):978.
    PMID: 39269555 DOI: 10.1007/s11033-024-09895-7
    BACKGROUND: Tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is an apoptosis inducer that exhibits an ideal therapeutic safety profile with less adverse effects than conventional chemotherapy. However, the occurrence of TRAIL resistance has been reported in various cancers including colorectal cancer (CRC). Substantial efforts have been channelled towards managing TRAIL resistance including identifying molecular targets. Interleukins (ILs) have been recently shown to play critical roles in modulating TRAIL sensitivity in cancer cells.

    METHODS AND RESULTS: This study investigated the roles of two ILs, IL-8 and IL⍺, in TRAIL resistance in CRC. TRAIL-resistant HT-29 and TRAIL-sensitive HCT 116 cells, were treated with human recombinant IL-8 and IL-1⍺. The results indicated that treatment with IL-8 (2.5 ng/mL) significantly protected TRAIL-sensitive HCT 116 cells from TRAIL-induced cell death (p cell death. By inhibiting its activation with wortmannin, the protective role of IL-8 against TRAIL treatment was reversed, suggesting the involvement of the PI3K pathway.

    CONCLUSION: Collectively, findings from this study identified the role of IL-8 and PI3K in modulating CRC cells' sensitivity to TRAIL. Further validation of these two potential molecular targets is warranted to overcome TRAIL resistance in CRC.

    Matched MeSH terms: Cell Death/drug effects
  11. Fulltext Cytotoxic effect of commonly used food dyes on human Hepatoma cell line, HepG2
    Lye, H.M., Chiew, J.C., Siddique, M.M.
    International Food Research Journal, 2018;25(4):1457-1463.
    MyJurnal
    The increasing and widespread use of synthetic food dyes raises health concerns and earlier reports suggest that certain food dyes might be harmful for human health. In this study, we have investigated the effect of three commonly used food dyes on human liver cell line, HepG2. Our findings suggest that these experimental food dyes significantly affect cell viability and this effect can be worsen in hyperglycemic condition. Accumulation of cellular fat was significantly higher in presence of these dyes. Expression pattern of the gene involved in regulating apoptosis suggests that that the observed cell death could be attributed to the activation of apoptotic pathway. These findings suggest that these experimental dyes might exert synergistic toxicity in hyperglycemia that need to be confirmed using suitable in vivo models.
    Matched MeSH terms: Cell Death
  12. Toxicity assessment of reduced graphene oxide and titanium dioxide nanomaterials on gram-positive and gram-negative bacteria under normal laboratory lighting condition
    Ahmad NS, Abdullah N, Yasin FM
    Toxicol Rep, 2020;7:693-699.
    PMID: 32528857 DOI: 10.1016/j.toxrep.2020.04.015
    Toxicity effect of reduced graphene oxide (rGO) and titanium dioxide (TiO2) nanomaterials (NMs) on Gram-positive (Bacillus subtilis) and Gram-negative (Escherichia coli) bacteria was assessed. For both strains, study demonstrated that the toxicity was time and concentration dependent which led to reduction in growth rate and cell death. Upon NMs exposure, an instantaneous cell death in E. coli culture was observed. This is in contrast with B. subtilis, in which the culture growth remained in the log phase; however their growth rate constant,

    μ
    g

    was reduced by ∼70%. The discrepancy between E. coli and B. subtilis was due to strain-specific response upon contact with NMs. TEM, SEM and EDX analysis revealed direct physical surface-surface interaction, as evidence from the adherence of NMs on the cell surface.
    Matched MeSH terms: Cell Death
  13. Fulltext In silico identification and in vitro assessment of a potential anti-breast cancer activity of antimicrobial peptide retrieved from the ATMP1 Anabas testudineus fish peptide
    Law D, Abdulkareem Najm A, Chong JX, K'ng JZY, Amran M, Ching HL, et al.
    PeerJ, 2023;11:e15651.
    PMID: 37483971 DOI: 10.7717/peerj.15651
    A previous study has shown that synthetic antimicrobial peptides (AMPs) derived from Anabas testudineus (ATMP1) could in-vitro inhibit the progression of breast cancer cell lines. In this study, we are interested in studying altered versions of previous synthetic AMPs to gain some insight into the peptides functions. The AMPs were altered and subjected to bioinformatics prediction using four databases (ADP3, CAMP-R3, AMPfun, and ANTICP) to select the highest anticancer activity. The bioinformatics in silico analysis led to the selection of two AMPs, which are ATMP5 (THPPTTTTTTTTTTTYTAAPATTT) and ATMP6 (THPPTTTTTTTTTTTTTAAPARTT). The in silico analysis predicted that ATMP5 and ATMP6 have anticancer activity and lead to cell death. The ATMP5 and ATMP6 were submitted to deep learning databases (ToxIBTL and ToxinPred2) to predict the toxicity of the peptides and to (AllerTOP & AllergenFP) check the allergenicity. The results of databases indicated that AMPs are non-toxic to normal human cells and allergic to human immunoglobulin. The bioinformatics findings led to select the highest active peptide ATMP5, which was synthesised and applied for in-vitro experiments using cytotoxicity assay MTT Assay, apoptosis detection using the Annexin V FTIC-A assay, and gene expression using Apoptosis PCR Array to evaluate the AMP's anticancer activity. The antimicrobial activity is approved by the disc diffusion method. The in-vitro experiments analysis showed that ATMP5 had the activity to inhibit the growth of the breast cancer cell line (MDA-MB-231) after 48 h and managed to arrest the cell cycle of the MDA-MB-231, apoptosis induction, and overexpression of the p53 by interaction with the related apoptotic genes. This research opened up new opportunities for developing potential and selective anticancer agents relying on antimicrobial peptide properties.
    Matched MeSH terms: Cell Death
  14. A Coxsackievirus B1-mediated nonlytic Extracellular Vesicle-to-cell mechanism of virus transmission and its possible control through modulation of EV release
    Jorfi S, Ansa-Addo EA, Mariniello K, Warde P, Bin Senian AA, Stratton D, et al.
    J Gen Virol, 2023 Sep;104(9).
    PMID: 37665326 DOI: 10.1099/jgv.0.001884
    Like most non-enveloped viruses, CVB1 mainly uses cell lysis to spread. Details of a nonlytic virus transmission remain unclear. Extracellular Vesicles (EVs) transfer biomolecules between cells. We show that CVB1 entry into HeLa cells results in apoptosis and release of CVB1-induced 'medium-sized' EVs (CVB1i-mEVs). These mEVs (100-300 nm) harbour CVB1 as shown by immunoblotting with anti-CVB1-antibody; viral capsids were detected by transmission electron microscopy and RT-PCR revealed CVB1 RNA. The percentage of mEVs released from CVB1-infected HeLa cells harbouring virus was estimated from TEM at 34 %. Inhibition of CVB1i-mEV production, with calpeptin or siRNA knockdown of CAPNS1 in HeLa cells limited spread of CVB1 suggesting these vesicles disseminate CVB1 virions to new host cells by a nonlytic EV-to-cell mechanism. This was confirmed by detecting CVB1 virions inside HeLa cells after co-culture with CVB1i-mEVs; EV release may also prevent apoptosis of infected cells whilst spreading apoptosis to secondary sites of infection.
    Matched MeSH terms: Cell Death
  15. The cathepsin B inhibitor z-FA-CMK induces cell death in leukemic T cells via oxidative stress
    Liow KY, Chow SC
    Naunyn Schmiedebergs Arch Pharmacol, 2018 Jan;391(1):71-82.
    PMID: 29085973 DOI: 10.1007/s00210-017-1436-6
    The cathepsin B inhibitor benzyloxycarbonyl-phenylalanine-alanine-chloromethyl ketone (z-FA-CMK) was recently found to induce apoptosis at low concentrations in Jurkat T cells, while at higher concentrations, the cells die of necrosis. In the present study, we showed that z-FA-CMK readily depletes intracellular glutathione (GSH) with a concomitant increase in reactive oxygen species (ROS) generation. The toxicity of z-FA-CMK in Jurkat T cells was completely abrogated by N-acetylcysteine (NAC), suggesting that the toxicity mediated by z-FA-CMK is due to oxidative stress. We found that L-buthionine sulfoximine (BSO) which depletes intracellular GSH through the inhibition of GSH biosynthesis in Jurkat T cells did not promote ROS increase or induce cell death. However, NAC was still able to block z-FA-CMK toxicity in Jurkat T cells in the presence of BSO, indicating that the protective effect of NAC does not involve GSH biosynthesis. This is further corroborated by the protective effect of the non-metabolically active D-cysteine on z-FA-CMK toxicity. Furthermore, in BSO-treated cells, z-FA-CMK-induced ROS increased which remains unchanged, suggesting that the depletion of GSH and increase in ROS generation mediated by z-FA-CMK may be two separate events. Collectively, our results demonstrated that z-FA-CMK toxicity is mediated by oxidative stress through the increase in ROS generation.
    Matched MeSH terms: Cell Death/drug effects; Cell Death/physiology
  16. Fulltext Functional validation of putative toxin-antitoxin genes from the Gram-positive pathogen Streptococcus pneumoniae: phd-doc is the fourth bona-fide operon
    Chan WT, Yeo CC, Sadowy E, Espinosa M
    Front Microbiol, 2014;5:677.
    PMID: 25538695 DOI: 10.3389/fmicb.2014.00677
    Bacterial toxin-antitoxin (TAs) loci usually consist of two genes organized as an operon, where their products are bound together and inert under normal conditions. However, under stressful circumstances the antitoxin, which is more labile, will be degraded more rapidly, thereby unleashing its cognate toxin to act on the cell. This, in turn, causes cell stasis or cell death, depending on the type of TAs and/or time of toxin exposure. Previously based on in silico analyses, we proposed that Streptococcus pneumoniae, a pathogenic Gram-positive bacterium, may harbor between 4 and 10 putative TA loci depending on the strains. Here we have chosen the pneumococcal strain Hungary(19A)-6 which contains all possible 10 TA loci. In addition to the three well-characterized operons, namely relBE2, yefM-yoeB, and pezAT, we show here the functionality of a fourth operon that encodes the pneumococcal equivalent of the phd-doc TA. Transcriptional fusions with gene encoding Green Fluorescent Protein showed that the promoter was slightly repressed by the Phd antitoxin, and exhibited almost background values when both Phd-Doc were expressed together. These findings demonstrate that phd-doc shows the negative self-regulatory features typical for an authentic TA. Further, we also show that the previously proposed TAs XreA-Ant and Bro-XreB, although they exhibit a genetic organization resembling those of typical TAs, did not appear to confer a functional behavior corresponding to bona fide TAs. In addition, we have also discovered new interesting bioinformatics results for the known pneumococcal TAs RelBE2 and PezAT. A global analysis of the four identified toxins-antitoxins in the pneumococcal genomes (PezAT, RelBE2, YefM-YoeB, and Phd-Doc) showed that RelBE2 and Phd-Doc are the most conserved ones. Further, there was good correlation among TA types, clonal complexes and sequence types in the 48 pneumococcal strains analyzed.
    Matched MeSH terms: Cell Death
  17. Fulltext Chlamydia and Its Many Ways of Escaping the Host Immune System
    Wong WF, Chambers JP, Gupta R, Arulanandam BP
    J Pathog, 2019;2019:8604958.
    PMID: 31467721 DOI: 10.1155/2019/8604958
    The increasing number of new cases of Chlamydia infection worldwide may be attributed to the pathogen's ability to evade various host immune responses. Summarized here are means of evasion utilized by Chlamydia enabling survival in a hostile host environment. The pathogen's persistence involves a myriad of molecular interactions manifested in a variety of ways, e.g., formation of membranous intracytoplasmic inclusions and cytokine-induced amino acid synthesis, paralysis of phagocytic neutrophils, evasion of phagocytosis, inhibition of host cell apoptosis, suppression of antigen presentation, and induced expression of a check point inhibitor of programmed host cell death. Future studies could focus on the targeting of these molecules associated with immune evasion, thus limiting the spread and tissue damage caused by this pathogen.
    Matched MeSH terms: Cell Death
  18. Fulltext Apoptosis: Dual Role in Aetiology and Cure
    Wynn, Aye Aye, Myint, Ohnmar, Mya, Nang Khin
    Borneo Journal of Medical Sciences, 2019;13(3):5-10.
    MyJurnal
    Apoptosis is a programmed cell death which occurs following a variety of stimuli. Physiologically the process is important for morphogenesis of organs and homeostasis of different types of cells. Apoptotic cell death is responsible for a variety of pathologic states such as elimination of cell death in mutated cells, infected cells, tumour cells and transplant rejection well as the pathological atrophy. In this review, there is discussion about the control of apoptosis, detection methods of apoptosis, its association with infectious and non-communicable diseases. Intracellular microorganisms survive through inhibition of host cell apoptosis as well as they destroy the parenchymal cells causing impaired functions. It plays important role in tumourigenesis. There are possible therapeutic roles of drugs that modify apoptosis in human diseases.
    Matched MeSH terms: Cell Death
  19. Role of α7 nicotinic acetylcholine receptor subtype in neuroprotection: an overview
    Muthuraju, S., Abdullah, J.M.
    Orient Neuron Nexus, 2011;2(1):10-14.
    MyJurnal
    Neuronal cell death results from various circumstances such as hypoxia, ischemic and neurodegenerative diseases (NDs). In these events, the resulting modification of neurotransmitters, either excitatory or inhibitory, mediate much of the neuronal damage. However, this consequence depends upon their pre and post synaptic receptor activities which are the key mechanism for signal regulation. Among these, acetylcholine (ACh) is a well known neurotransmitter which is predominantly involved in neuroprotection as well as cognitive functions through its receptors activity, particularly the nicotinic subtypes. Several lines of evidence suggest that among these subtypes, a7 nicotinic acetylcholine receptor (a7nAChR) offers much promise for neuroprotective role in relation to the central nervous system (CNS) disorders like schizophrenia and Alzheimer's disease (AD). Several lines of evidence exist to show the potential mechanisms in which this nAChR subtype and its agonists such as nicotine, that trigger the a7nAChR-mediated suppression of neuronal cell death. This review focuses on the potential role of a7nAChR in neuroprotection by examining recent experimental data, both in vitro and in vivo, that argue for the neuroprotective role of a7nAChR in the CNS.
    Matched MeSH terms: Cell Death
  20. Identification of differentially expressed genes in oil palms (Elaeis guineensis) related to infections by Ganoderma boninense
    Mohamad Arif, A.M., Zetty Norhana, B.Y., Abdullah, F., Tan, Su.G., Ismail, S.
    Buletin Persatuan Genetik Malaysia, 2005;11(2):0-0.
    MyJurnal
    Basal stem rot (BSR) caused by species Ganoderma, is one of the most serious disease of oil palm in Malaysia. As far as the disease problem to oil palm in Malaysia is concerned, BSR is the only disease requiring urgent solution. The BSR is not new to Malaysia, it has been known to attack oil palm since the early years when the crop was introduced into this country. There is an indication that there are differences in susceptibility to basal stem rot between germplasm materials from different genetic origin [2]. This provides hope in generating oil palm varieties with reduced level of susceptibility using existing genetic materials. There is also interest in developing diagnostic tools such as using PCR primers for detection of the pathogen in oil palms [1]. Altered expression of several classes of genes was observed in plants in response to fungal infection. These include genes associated with cell maintenance and development, genes involved in biosynthesis of lignin and phenolics and genes implicated in oxidative burst, programmed cell death or hypersensitive response [5].
    Matched MeSH terms: Cell Death
Related Terms
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links