hgprt การใช้

• The HGPRT deficiency causes a build-up of uric acid in all body fluids.
• HGPRT is a transferase that catalyzes conversion of hypoxanthine to inosine monophosphate and guanine to guanosine monophosphate.
• In this way, only the B cell-myeloma hybrids survive, since the HGPRT gene coming from the B cells is functional.
• It is possible for a female to inherit an X chromosome from her unaffected father, who carries a new mutation of the HGPRT gene.
• Decreased levels of hypoxanthine guanine phosphoribosyl transferase ( HGPRT ) causes this accumulation, as PRPP is a substrate used by HGPRT during purine salvage.
• Decreased levels of hypoxanthine guanine phosphoribosyl transferase ( HGPRT ) causes this accumulation, as PRPP is a substrate used by HGPRT during purine salvage.
• The Cobra virus also knocks out the gene for the enzyme hypoxanthine-guanine phosphoribosyltransferase ( HGPRT ), whose absence causes Lesch-Nyhan syndrome.
• Unfused myeloma cells cannot grow because they lack HGPRT and thus cannot replicate their DNA . Unfused spleen cells cannot grow indefinitely because of their limited life span.
• In this case hypoxanthine-guanine phosphoribosyltransferase ( HGPRT ) reacts hypoxanthine absorbed from the medium with PRPP, liberating pyrophosphate, to produce IMP by a salvage pathway.
• Thus, one may fuse HGPRT deficient human cells ( designated as TK + HGPRr-) with TK deficient mouse cells ( denoted as TK-HGPRT + ).
• Thus, one may fuse HGPRT deficient human cells ( designated as TK + HGPRr-) with TK deficient mouse cells ( denoted as TK-HGPRT + ).
• Hybridomas are immortal ( immune to cellular senescence ), HGPRT + cells that result from fusion of mortal, HGPRT + plasma cells and immortal, HGPRT  " myeloma cells.
• Hybridomas are immortal ( immune to cellular senescence ), HGPRT + cells that result from fusion of mortal, HGPRT + plasma cells and immortal, HGPRT  " myeloma cells.
• Hybridomas are immortal ( immune to cellular senescence ), HGPRT + cells that result from fusion of mortal, HGPRT + plasma cells and immortal, HGPRT  " myeloma cells.
• Hybridoma cells can also be isolated using the same principle as described with respect to another gene the HGPRT, which synthesizes IMP necessary for GMP nucleotide synthesis in the salvage pathway.
• Thus, a cell lacking TK is resistant to bromodeoxyuridine ( BrdU ) and a cell lacking HGPRT is resistant to 6-thioguanine ( 6-TG ) and 8-azaguanine.
• Hypoxanthine is converted into guanine by the enzyme hypoxanthine-guanine phosphoribosyltransferase ( HGPRT ), while thymidine is phosphorylated by thymidine kinase ( TK ); both HGPRT and TK are enzymes of the salvage pathway.
• Hypoxanthine is converted into guanine by the enzyme hypoxanthine-guanine phosphoribosyltransferase ( HGPRT ), while thymidine is phosphorylated by thymidine kinase ( TK ); both HGPRT and TK are enzymes of the salvage pathway.
• For using HAT medium as a selective agent, human cells used for fusion must be deficient for either the enzyme HGPRT or TK, while mouse cells must be deficient for the other enzyme of this pair.
• The myeloma cells are selected beforehand to ensure they are not secreting antibody themselves and that they lack the hypoxanthine-guanine phosphoribosyltransferase ( HGPRT ) gene, making them sensitive to the HAT medium ( see below ).