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Articles by Mujahid Khalaf Ali
Total Records ( 2 ) for Mujahid Khalaf Ali
  Mujahid Khalaf Ali
  To exhibit an incorporated atomic science devoted system for tuberculosis diagnosis. Mycobacterium tuberculosis (MTB) instigates putrefaction of infected cells to avoid immune reactions. As of late we found that MTB uses the protein CpnT to execute human macrophages by discharging its C-terminal area, named Tuberculosis Necrotizing Toxin (TNT) that incites putrefaction by an obscure component. The TNT controls the cytosol of MTB-infected macrophages where it hydrolyzes the main element co-catalyst Nicotinamide Adenine Dinucleotide (NAD+). Articulation or infusion of a non-synergist TNT mutant demonstrated no cytotoxicity in macrophages or zebrafish zygotes, separately, exhibiting that the NAD+-glycohydrolase action is required for TNT-prompted cell demise. To anticipate self-harming, MTB produces a Immunity Factor for TNT (IFT) that ties TNT and represses its action. The precious stone structure of the TNT-IFT complex uncovered a novel NAD+-glycohydrolase overlap of TNT which constitutes the establishing individual from a toxin family across the board in pathogenic micro-organisms.
  Mujahid Khalaf Ali
  Exotoxin A is an extracellular compound that is delivered by most clinical strains of PPseudomonas aeruginosa. It is a solitary chain polypeptide (Atomic weight, 71,000) with A and B pieces that intercede enzymatic and cell-restricting capacities, individually. Exotoxin A catalyzes the exchange of the adenosine diphosphate-ribosyl moiety from nicotinamide-adenine dinucleotide to lengthening factor 2 which brings about the inactivation of the last mentioned and the restraint of protein biosynthesis. This enzymatic action (ADP-ribosyl [ADPR]-transferase) is thought to represent the poisonous quality of exotoxin A. The appropriation of the declaration of exotoxin an inside Pseudomonas animal varieties was inspected. Research center strains and clinical detaches of PPseudomonas aeruginosa were tried. The generation of exotoxin A was dictated by examining for ADPR-transferase movement in dialyzed solidified (-20°C) and defrosted without cell supernatants from 22-h societies or in 10-crease concentrated supernatants. The poison applied a stamped impact on the liver yet, evoked no self-evident minuscule changes in different organs. The infinitesimal injuries caused in the liver by a solitary infusion of two half deadly dosages (LD50) of poison (2.3~g) were portrayed by rot, cell swelling and greasy change inside 4-8 h and close aggregate hepatocellular necrosis at 48 h.
 
 
 
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