Skills (75)
Research experience
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Apr 2011–
presentResearch: University of Health Sciences
University of Health Sciences · Incharge Resource Lab · Molecular biology,pathology virology ImmunologyPakistan · LahoreAssistant Professor in UHS -
Mar 2011–
May 2012Research: Assistant professor, IMMUNOLOGY expertise in Molecular biology and virology HCV
University of Health Sciences, Pakistan,Lahore · Immunology · HCV Molecular virology cancer biology PhysiologyPakistan · Lahore -
Feb 2010–
Apr 2011Research: Cancer Biology, Molecular Mechanism of Breast cancer and Ovarian cancer...HPV genotyping
shoukat khanum memorial cancer hospital and Research centerrr · Cancer research center · Cancer Research groupPakistan · lahoreDr shah worked in Shukat khanum memorial cancer hospital from Feb 2010 to March 2011.... -
Jan 2010–
Dec 2012Research: University of the Punjab
University of the PunjabPakistan · Lahore -
Jan 2009–
Dec 2011Research: Centre of Excellence in Molecular Biology
Centre of Excellence in Molecular Biology · Virolgy and Functional GenomicsPakistan · lahore
Education
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Jan 2005–
Jan 2009CEMB National Center of Excellence in Molecular Biology Punjab university Lahore
Molecular Biology/Virology · PhDPakistan · Lahore
Awards & achievements
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Apr 2011Grant: HEC projct and HEC approved Supervisor
Other
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LanguagesEnglish, Urdu, Sraikee, Punjabi
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Scientific MembershipsPakistan Bio safety association, Gene therapy Association, European association cancer research,
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Journal RefereesBiological and Bio medical Reports, BMC Clinical Pathology, IJVAM
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Other InterestsNet Browsing, Book Reading
Questions and Answers (6) View all
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Answer added in RNA110 What is the best way to store RNA?it depends on the duration for which you want to store fore 1-3 days we can stoe at -20 and if you want to store for longer time thevWell we use DEPC ... [more]
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Question asked in Recombinant Technology1 How can commercially produced recombinant Epo in CHO Cell line be analyzed for bio-activity or bio availability?How can commercially produced recombinant Epo in CHO Cell line be analyzed for bio-activity or bio availability?
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Answer added in PCR1 Anyone with experience on Biorad IQ5 real time PCR machine?Yes it is possible to use different calibration files and all depend on your plates , wells setting and reagents (dyes) for callibration and specific ... [more]
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Answer added in ELISPOT12 Trouble with leaky ELISPOT platesPre wetting the whole plate PVDF is better option to get good transfer than nitrocellolose so try it
Publications (29) View all
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Article: Hepatitis C virus entry: Role of host and viral factors.
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ABSTRACT: Hepatitis C virus (HCV) has been considered to be a significant risk factor in developing liver associated diseases including hepatocellular carcinoma all over the world. HCV is an enveloped positive strand virus comprising a complex between genomic RNA and viral envelope glycoproteins (E1 and E2), which are anchored within host derived double-layered lipid membrane surrounding the nucleocapsid composed of several copies of core protein. HCV cell entry is the first step in infection and viral replication into host cells mainly hepatocytes. HCV cell entry is a complex process involving both the viral (envelope glycoproteins E1/E2) and host factors (cellular receptors and associated factors i.e. CD81, SR-BI, LDL-R, CLDN1, Occludin, DC-SIGN, L-SIGN and Glycosaminoglycans). Besides these the expression of certain other conditions such as polarization and EWI-2 expression inhibits the viral cell entry. Exploring the mechanism of HCV entry will help to better understand the viral life cycle and possible therapeutic targets against HCV infection including viral and host factors involved in this process. New strategies such as RNAi represents a new option for targeting the host or viral factors for prevention and therapeutic against HCV infection. In the current review we try to summarize the current knowledge about mechanism and interaction of cellular and viral factors involved in HCV cell entry and its implication as therapeutic target to inhibit HCV infection.Infection, genetics and evolution: journal of molecular epidemiology and evolutionary genetics in infectious diseases 08/2012; 12(8):1699-1709. · 3.22 Impact Factor -
Article: Hepatitis C virus to hepatocellular carcinoma.
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ABSTRACT: Hepatitis C virus causes acute and chronic hepatitis and can lead to permanent liver damage and hepatocellular carcinoma (HCC) in a significant number of patients via oxidative stress, insulin resistance (IR), fibrosis, liver cirrhosis and HCV induced steatosis. HCV induced steatosis and oxidative stress causes steato-hepatitis and these pathways lead to liver injury or HCC in chronic HCV infection. Steatosis and oxidative stress crosstalk play an important role in liver damage in HCV infection. This Review illustrates viral and host factors which induce Oxidative stress, steatosis and leads toward HCC. It also expresses Molecular cascade which leads oxidative stress and steatosis to HCC.Infectious Agents and Cancer 01/2012; 7(1):2. -
Article: Highly Pathogenic Avian Influenza Virus among Wild Birds in Mongolia
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ABSTRACT: Mongolia combines a near absence of domestic poultry, with an abundance of migratory waterbirds, to create an ideal location to study the epidemiology of highly pathogenic avian influenza virus (HPAIV) in a purely wild bird system. Here we present the findings of active and passive surveillance for HPAIV subtype H5N1 in Mongolia from 2005–2011, together with the results of five outbreak investigations. In total eight HPAIV outbreaks were confirmed in Mongolia during this period. Of these, one was detected during active surveillance employed by this project, three by active surveillance performed by Mongolian government agencies, and four through passive surveillance. A further three outbreaks were recorded in the neighbouring Tyva Republic of Russia on a lake that bisects the international border. No HPAIV was isolated (cultured) from 7,855 environmental fecal samples (primarily from ducks), or from 2,765 live, clinically healthy birds captured during active surveillance (primarily shelducks, geese and swans), while four HPAIVs were isolated from 141 clinically ill or dead birds located through active surveillance. Two low pathogenic avian influenza viruses (LPAIV) were cultured from ill or dead birds during active surveillance, while environmental feces and live healthy birds yielded 56 and 1 LPAIV respectively. All Mongolian outbreaks occurred in 2005 and 2006 (clade 2.2), or 2009 and 2010 (clade 2.3.2.1); all years in which spring HPAIV outbreaks were reported in Tibet and/or Qinghai provinces in China. The occurrence of outbreaks in areas deficient in domestic poultry is strong evidence that wild birds can carry HPAIV over at least moderate distances. However, failure to detect further outbreaks of clade 2.2 after June 2006, and clade 2.3.2.1 after June 2010 suggests that wild birds migrating to and from Mongolia may not be competent as indefinite reservoirs of HPAIV, or that HPAIV did not reach susceptible populations during our study. This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. Funding: Support for this project was provided by the National Institute of Allergy and Infectious Disease, National Institutes of Health, Department of Health and Human Services (Contracts HHSN266200700007C, HHSN266200700009C, and HHSN266200700005C), the United States Agency for International Development (USAID), the World Bank, and the Food and Agriculture Organization of the United Nations. DOJ was supported by generous funding from the Dunemere private foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: DOJ was supported by generous funding from the Dunemere private foundation. This does not alter the authors' adherence to all the PLoS ONE policies on sharing data and materials.PLoS ONE 01/2012; 7(9):e44097. · 4.09 Impact Factor -
Article: Anti-apoptotic effect of HCV core gene of genotype 3a in Huh-7 cell line.
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ABSTRACT: Hepatitis C virus (HCV) Core protein regulates multiple signaling pathways and alters cellular genes expression responsible for HCV induced pathogenesis leading to hepatocellular carcinoma (HCC). Prevalence of HCV genotype 3a associated HCC is higher in Pakistan as compare to the rest of world; however the molecular mechanism behind this is still unclear. This study has been designed to evaluate the effect of HCV core 3a on apoptosis and cell proliferation which are involved in HCC METHODOLOGY: We examined the in vitro effect of HCV Core protein of genotype 3a and 1a on cellular genes involved in apoptosis by Real time PCR in liver cell line (Huh-7). We analyzed the effect of HCV core of genotype 1a and 3a on cell proliferation by MTT assay and on phosphrylation of Akt by western blotting in Huh-7 cells. The HCV 3a Core down regulates the gene expression of Caspases (3, 8, 9 and 10), Cyto C and p53 which are involved in apoptosis. Moreover, HCV 3a Core gene showed stronger effect in regulating protein level of p-Akt as compared to HCV 1a Core accompanied by enhanced cell proliferation in Huh-7 cell line. From the current study it has been concluded that reduced expression of cellular genes involved in apoptosis, increased p-Akt (cell survival gene) and enhanced cell proliferation in response to HCV 3a core confirms anti apoptotic effect of HCV 3a Core gene in Huh-7 that may lead to HCC.Virology Journal 11/2011; 8:522. · 2.34 Impact Factor -
Article: Inhibition of HCV 3a genotype entry through host CD81 and HCV E2 antibodies.
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ABSTRACT: HCV causes acute and chronic hepatitis which can eventually lead to permanent liver damage hepatocellular carcinoma and death. HCV glycoproteins play an important role in HCV entry by binding with CD81 receptors. Hence inhibition of virus at entry step is an important target to identify antiviral drugs against HCV. The present study elaborated the role of CD81 and HCV glycoprotein E2 in HCV entry using retroviral pseudo-particles of 3a local genotype. Our results demonstrated that HCV specific antibody E2 and host antibody CD81 showed dose- dependent inhibition of HCV entry. HCV E2 antibody showed 50% reduction at a concentration of 1.5 ± 1 μg while CD81 exhibited 50% reduction at a concentration of 0.8 ± 1 μg. In addition, data obtained with HCVpp were also confirmed with the infection of whole virus of HCV genotype 3a in liver cells. Our data suggest that HCV specific E2 and host CD81 antibodies reduce HCVpp entry and full length viral particle and combination of host and HCV specific antibodies showed synergistic effect in reducing the viral titer.Journal of Translational Medicine 11/2011; 9:194. · 3.41 Impact Factor
