中国人肠道产甲酸草酸杆菌甲酰辅酶A转移酶和草酰辅酶A脱羧酶基因的克隆及其在真核细胞中的表达研究
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摘要
目的:草酸(Oxalic Acid, Oxalate)是机体不能进一步分解代谢的终产物,对组织细胞具有一定的毒性。一般情况下,来自于机体代谢的内源性草酸(主要在肝脏内合成)和肠道从食物中吸收的外源性草酸(包括草酸前体物质)均以草酸原形形式从尿中排泄。肝脏合成的异常增加和肠道的高吸收是高草酸尿的发病基础。产甲酸草酸杆菌(Oxalobacter formigenes, Ox.F)是一种定居于脊柱动物肠道,与宿主形成共生关系的正常菌群(flora),具有分解草酸、调节外源性草酸吸收的功能。甲酰辅酶A转移酶基因(frc)是Ox.F分解草酸的关键酶基因之一。本研究通过真核表达载体克隆产甲酸草酸杆菌frc基因,以探讨重组frc基因能否在在真核细胞中表达,为高草酸尿的基因治疗奠定基础。
方法:提取中国人肠道产甲酸草酸杆菌的基因组DNA,用聚合酶链式反应(Polymerase Chain Reaction,PCR)技术从产甲酸草酸杆菌基因组DNA中扩增frc基因片段并插入真核表达载体pEGFP-C1,获取重组质粒pEGFP-frc,通过限制性内切酶酶切电泳和测序鉴定重组质粒。重组质粒转染人胚肾293细胞,通过逆转录PCR(Reverse Transcription PCR,RT-PCR)和蛋白印迹(Western blot)分别从mRNA和蛋白水平检测frc基因在真核细胞中的表达。被转染细胞在含草酸培养液中培养,检测0~72h培养液中草酸浓度的变化。
结果:中国人肠道产甲酸草酸杆菌frc基因全长1287bp,存在53个碱基和4个氨基酸残基的变异,与GenBank中的frc基因的碱基序列的同源性为95.88%,氨基酸残基序列的同源性为99.07%。转染HEK293细胞后24~72小时,可观察到明亮的绿色荧光,RT-PCR和Western blot分别从mRNA和蛋白水平上检测到frc基因在真核细胞中的表达。转染pEGFP-frc细胞12~72h培养液中草酸浓度明显低于转染空载体的细胞(P<0.05)。
结论:中国人肠道产甲酸草酸杆菌中可分离出frc基因;中国人肠道产甲酸草酸杆菌frc基因存在一定的变异;frc基因可在真核细胞HEK293细胞中表达并使HEK293细胞获得代谢草酸的能力。
目的:草酸(Oxalic Acid, Oxalate)是机体不能进一步分解代谢的终产物,对组织细胞具有一定的毒性。一般情况下,来自于机体代谢的内源性草酸(主要在肝脏内合成)和肠道从食物中吸收的外源性草酸(包括草酸前体物质)均以草酸原形形式从尿中排泄。肝脏合成的异常增加和肠道的高吸收是高草酸尿的发病基础。产甲酸草酸杆菌(Oxalobacter formigenes, Ox.F)是一种定居于脊柱动物肠道,与宿主形成共生关系的正常菌群(flora),具有分解草酸、调节外源性草酸吸收的功能。草酰辅酶A脱羧酶基因(oxc)是Ox.F分解草酸的关键酶基因之一。本研究通过真核表达载体克隆产甲酸草酸杆菌oxc基因,以探讨中国人肠道产甲酸草酸杆菌(Ox.F)草酰辅酶A脱羧酶基因(oxc)的分离、克隆及其在293细胞中的表达,为高草酸尿的基因治疗奠定基础。
方法:提取中国人肠道Ox.F的基因组DNA,PCR扩增oxc基因片段并克隆入真核表达载体pEGFP-C1,通过限制性内切酶酶切电泳和测序鉴定基因片段。将重组质粒脂质体转染至人胚肾293细胞,通过逆转录PCR(Reverse Transcription PCR,RT-PCR)和蛋白印迹(Western blot)分别从mRNA和蛋白水平检测oxc基因在真核细胞中的表达。
结果:中国人肠道产甲酸草酸杆菌oxc基因全长1707bp。与GenBank中的序列比较,存在109个碱基的变异,同源性为93.61%,由于密码子的简并性,表达产物将出现16个氨基酸残基的变异,同源性为97.18%。重组质粒转染293细胞后24~48h,可观察到明亮的绿色荧光,从mRNA和蛋白水平上可以检测到oxc基因在真核细胞中的表达。
结论:中国人肠道产甲酸草酸杆菌中可以分离出oxc基因;中国人肠道产甲酸草酸杆菌oxc基因存在一定的变异;oxc基因可在真核细胞293细胞中表达。
Objective: Oxalate is a highly toxic natural byproduct of normal cellular metabolism. Abnormally synthesis major in liver or hyperabsorption in gut of oxalate can lead to the accumulation of oxalate in vivo and result in disorder of oxalate metabolism, hyperoxaluria. To study the molecular cloning, identification and expression of frc, the formyl-CoA transferase (frc) gene of Oxalobacter formigenes from the intestines of Chinese people was subcloned to a eukaryotic expression vector and the expression of frc gene was identified.
Methods: The genomic DNA of Oxalobacter formigenes was extracted from the intestines of Chinese people. The fragment of frc gene was amplified by polymerase chain reaction and was linked with eukaryotic expression vector pEGFP-C1. The recombinant plasmid was named as pEGFP-frc and was identified by restriction-enzyme cutting and sequencing. Human embryo kidney 293 cells were transfected with the recombinated plasmid pEGFP-frc by LipofectamineTM 2000. RT-PCR was performed to detect the mRNA express of frc. Western blot were performed to detect the fusion protein express of FCoAT-EGFP. The transfected cells were cultured in oxalate-contained medium and the concentration of oxalate was measured at 0~72 h.
Results: The total length of frc gene from Oxalobacter formigenes in the intestines of Chinese people was 1287 bp, and there were mutation of 53 nucleotides and 4 amino-acid residue. The homology of nucleotides and amino-acid residue with the sequence in GenBank was 95.88% and 99.07%. The recombinant eukaryotic expression vector was constructed successfully. Relucent green fluorescence emerged from HEK293 cells 24~72 h after transfection. The frc mRNA and fusion protein were detected from the cell transfected. The concentration of oxalate in the medium of pEGFP-frc transfected cell was lower than that of pEGFP-C1 transfected cell at 12~72h (P<0.05).
Conclusion: The frc gene can be cloned from the Oxalobacter formigenes in the intestines of Chinese people and there are some mutation with the frc gene. The mutation frc gene can express in eucaryotic cell.
Objective: Oxalate is a highly toxic natural byproduct of normal cellular metabolism. Abnormally synthesis major in liver or hyperabsorption in gut of oxalate can lead to the accumulation of oxalate in vivo and result in disorder of oxalate metabolism, hyperoxaluria. To study the cloning and identification of oxc gene from Oxalobacter formigenes in the intestines of Chinese people, the oxalyl-CoA decarboxylase (oxc) gene of Oxalobacter formigenes was subcloned to a eukaryotic expression vector and the expression of oxc gene was identified.
Methods: The genomic DNA of Oxalobacter formigenes was extracted from the intestines of Chinese people. The fragment of oxc gene was amplified by polymerase chain reaction and was linked with eukaryotic expression vector pEGFP-C1. The fragment of oxc gene was identified by restriction-enzyme cutting and sequencing. Human embryo kidney 293 cells were transfected with the recombinated plasmid by LipofectamineTM 2000. RT-PCR were performed to detect the mRNA express of oxc. Western blot were performed to detect the fusion protein express of OCoAD-EGFP.
Results: The total length of oxc gene from Oxalobacter formigenes in the intestines of Chinese people was 1707bp, and there were mutation of 109 nucleotides and 16 amino-acid residue. The homology of nucleotides and amino-acid residue with the sequence in GenBank was 93.61% and 97.18%. 293 cells transfected with the recombinated plasmid expressed relucent green fluorescence. The mRNA of oxc gene was detected by RT-PCR with a 347bp amplified product. The fusion protein express of OCoAD-EGFP was detected by Western blot with a 90kD protein.
Conclusion: The oxc gene can be cloned from the Oxalobacter formigenes in the intestines of Chinese people and there are some mutation with the oxc gene. The mutation oxc gene can express in eucaryotic cell.
方法:提取中国人肠道产甲酸草酸杆菌的基因组DNA,用聚合酶链式反应(Polymerase Chain Reaction,PCR)技术从产甲酸草酸杆菌基因组DNA中扩增frc基因片段并插入真核表达载体pEGFP-C1,获取重组质粒pEGFP-frc,通过限制性内切酶酶切电泳和测序鉴定重组质粒。重组质粒转染人胚肾293细胞,通过逆转录PCR(Reverse Transcription PCR,RT-PCR)和蛋白印迹(Western blot)分别从mRNA和蛋白水平检测frc基因在真核细胞中的表达。被转染细胞在含草酸培养液中培养,检测0~72h培养液中草酸浓度的变化。
结果:中国人肠道产甲酸草酸杆菌frc基因全长1287bp,存在53个碱基和4个氨基酸残基的变异,与GenBank中的frc基因的碱基序列的同源性为95.88%,氨基酸残基序列的同源性为99.07%。转染HEK293细胞后24~72小时,可观察到明亮的绿色荧光,RT-PCR和Western blot分别从mRNA和蛋白水平上检测到frc基因在真核细胞中的表达。转染pEGFP-frc细胞12~72h培养液中草酸浓度明显低于转染空载体的细胞(P<0.05)。
结论:中国人肠道产甲酸草酸杆菌中可分离出frc基因;中国人肠道产甲酸草酸杆菌frc基因存在一定的变异;frc基因可在真核细胞HEK293细胞中表达并使HEK293细胞获得代谢草酸的能力。
目的:草酸(Oxalic Acid, Oxalate)是机体不能进一步分解代谢的终产物,对组织细胞具有一定的毒性。一般情况下,来自于机体代谢的内源性草酸(主要在肝脏内合成)和肠道从食物中吸收的外源性草酸(包括草酸前体物质)均以草酸原形形式从尿中排泄。肝脏合成的异常增加和肠道的高吸收是高草酸尿的发病基础。产甲酸草酸杆菌(Oxalobacter formigenes, Ox.F)是一种定居于脊柱动物肠道,与宿主形成共生关系的正常菌群(flora),具有分解草酸、调节外源性草酸吸收的功能。草酰辅酶A脱羧酶基因(oxc)是Ox.F分解草酸的关键酶基因之一。本研究通过真核表达载体克隆产甲酸草酸杆菌oxc基因,以探讨中国人肠道产甲酸草酸杆菌(Ox.F)草酰辅酶A脱羧酶基因(oxc)的分离、克隆及其在293细胞中的表达,为高草酸尿的基因治疗奠定基础。
方法:提取中国人肠道Ox.F的基因组DNA,PCR扩增oxc基因片段并克隆入真核表达载体pEGFP-C1,通过限制性内切酶酶切电泳和测序鉴定基因片段。将重组质粒脂质体转染至人胚肾293细胞,通过逆转录PCR(Reverse Transcription PCR,RT-PCR)和蛋白印迹(Western blot)分别从mRNA和蛋白水平检测oxc基因在真核细胞中的表达。
结果:中国人肠道产甲酸草酸杆菌oxc基因全长1707bp。与GenBank中的序列比较,存在109个碱基的变异,同源性为93.61%,由于密码子的简并性,表达产物将出现16个氨基酸残基的变异,同源性为97.18%。重组质粒转染293细胞后24~48h,可观察到明亮的绿色荧光,从mRNA和蛋白水平上可以检测到oxc基因在真核细胞中的表达。
结论:中国人肠道产甲酸草酸杆菌中可以分离出oxc基因;中国人肠道产甲酸草酸杆菌oxc基因存在一定的变异;oxc基因可在真核细胞293细胞中表达。
Objective: Oxalate is a highly toxic natural byproduct of normal cellular metabolism. Abnormally synthesis major in liver or hyperabsorption in gut of oxalate can lead to the accumulation of oxalate in vivo and result in disorder of oxalate metabolism, hyperoxaluria. To study the molecular cloning, identification and expression of frc, the formyl-CoA transferase (frc) gene of Oxalobacter formigenes from the intestines of Chinese people was subcloned to a eukaryotic expression vector and the expression of frc gene was identified.
Methods: The genomic DNA of Oxalobacter formigenes was extracted from the intestines of Chinese people. The fragment of frc gene was amplified by polymerase chain reaction and was linked with eukaryotic expression vector pEGFP-C1. The recombinant plasmid was named as pEGFP-frc and was identified by restriction-enzyme cutting and sequencing. Human embryo kidney 293 cells were transfected with the recombinated plasmid pEGFP-frc by LipofectamineTM 2000. RT-PCR was performed to detect the mRNA express of frc. Western blot were performed to detect the fusion protein express of FCoAT-EGFP. The transfected cells were cultured in oxalate-contained medium and the concentration of oxalate was measured at 0~72 h.
Results: The total length of frc gene from Oxalobacter formigenes in the intestines of Chinese people was 1287 bp, and there were mutation of 53 nucleotides and 4 amino-acid residue. The homology of nucleotides and amino-acid residue with the sequence in GenBank was 95.88% and 99.07%. The recombinant eukaryotic expression vector was constructed successfully. Relucent green fluorescence emerged from HEK293 cells 24~72 h after transfection. The frc mRNA and fusion protein were detected from the cell transfected. The concentration of oxalate in the medium of pEGFP-frc transfected cell was lower than that of pEGFP-C1 transfected cell at 12~72h (P<0.05).
Conclusion: The frc gene can be cloned from the Oxalobacter formigenes in the intestines of Chinese people and there are some mutation with the frc gene. The mutation frc gene can express in eucaryotic cell.
Objective: Oxalate is a highly toxic natural byproduct of normal cellular metabolism. Abnormally synthesis major in liver or hyperabsorption in gut of oxalate can lead to the accumulation of oxalate in vivo and result in disorder of oxalate metabolism, hyperoxaluria. To study the cloning and identification of oxc gene from Oxalobacter formigenes in the intestines of Chinese people, the oxalyl-CoA decarboxylase (oxc) gene of Oxalobacter formigenes was subcloned to a eukaryotic expression vector and the expression of oxc gene was identified.
Methods: The genomic DNA of Oxalobacter formigenes was extracted from the intestines of Chinese people. The fragment of oxc gene was amplified by polymerase chain reaction and was linked with eukaryotic expression vector pEGFP-C1. The fragment of oxc gene was identified by restriction-enzyme cutting and sequencing. Human embryo kidney 293 cells were transfected with the recombinated plasmid by LipofectamineTM 2000. RT-PCR were performed to detect the mRNA express of oxc. Western blot were performed to detect the fusion protein express of OCoAD-EGFP.
Results: The total length of oxc gene from Oxalobacter formigenes in the intestines of Chinese people was 1707bp, and there were mutation of 109 nucleotides and 16 amino-acid residue. The homology of nucleotides and amino-acid residue with the sequence in GenBank was 93.61% and 97.18%. 293 cells transfected with the recombinated plasmid expressed relucent green fluorescence. The mRNA of oxc gene was detected by RT-PCR with a 347bp amplified product. The fusion protein express of OCoAD-EGFP was detected by Western blot with a 90kD protein.
Conclusion: The oxc gene can be cloned from the Oxalobacter formigenes in the intestines of Chinese people and there are some mutation with the oxc gene. The mutation oxc gene can express in eucaryotic cell.
引文
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[1]叶章群.泌尿系结石研究现况与展望.中华实验外科杂志2005;22: 261-262.
[2] Tiselius HG. Stone incidence and prevention. Braz J Urol 2000;26: 452-462.
[3] Chen Z, Ye Z, Zeng L, Yang W. Clinical investigation on gastric oxalate absorption. Chin Med J (Engl) 2003;116: 1749-1751.
[4] Sidhu H, Schmidt ME, Cornelius JG, Thamilselvan S, Khan SR, Hesse A, Peck AB. Direct correlation between hyperoxaluria/oxalate stone disease and the absence of the gastrointestinal tract-dwelling bacterium Oxalobacter formigenes: possible prevention by gut recolonization or enzyme replacement therapy. J Am Soc Nephrol 1999;10 Suppl 14: S334-40.
[5] Allison MJ, Dawson KA, Mayberry WR, Foss JG. Oxalobacter formigenes gen. nov., sp. nov.: oxalate-degrading anaerobes that inhabit the gastrointestinal tract. Arch Microbiol 1985;141: 1-7.
[6]陈志强,郭辉,叶章群,朱旭慧,余建华,曾令启.人肠道产甲酸草酸杆菌的分离培养.中华实验外科杂志2005;22: 1402-1403.
[7] Mittal RD, Kumar R. Gut-inhabiting bacterium Oxalobacter formigenes: role in calcium oxalate urolithiasis. J Endourol 2004;18: 418-24.
[8] Sidhu H, Allison M, Peck AB. Identification and classification of Oxalobacter formigenes strains by using oligonucleotide probes and primers. J Clin Microbiol 1997;35: 350-3.
[9] Baetz AL, Allison MJ. Purification and characterization of oxalyl-coenzyme A decarboxylase from Oxalobacter formigenes. J Bacteriol 1989;171: 2605-8.
[10] Baetz AL, Allison MJ. Purification and characterization of formyl-coenzyme A transferase from Oxalobacter formigenes. J Bacteriol 1990;172: 3537-40.
[11] Lung HY, Cornelius JG, Peck AB. Cloning and expression of the oxalyl-CoA decarboxylase gene from the bacterium, Oxalobacter formigenes: prospects for genetherapy to control Ca-oxalate kidney stone formation. Am J Kidney Dis 1991;17: 381-5.
[12] Lung HY, Baetz AL, Peck AB. Molecular cloning, DNA sequence, and gene expression of the oxalyl-coenzyme A decarboxylase gene, oxc, from the bacterium Oxalobacter formigenes. J Bacteriol 1994;176: 2468-72.
[13] Sidhu H, Ogden SD, Lung HY, Luttge BG, Baetz AL, Peck AB. DNA sequencing and expression of the formyl coenzyme A transferase gene, frc, from Oxalobacter formigenes. J Bacteriol 1997;179: 3378-81.
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[15] Kwak C, Jeong BC, Kim HK, Kim EC, Chox MS, Kim HH. Molecular epidemiology of fecal Oxalobacter formigenes in healthy adults living in Seoul, Korea. J Endourol 2003;17: 239-43.
[16] Gruez A, Roig-Zamboni V, Valencia C, Campanacci V, Cambillau C. The crystal structure of the Escherichia coli YfdW gene product reveals a new fold of two interlaced rings identifying a wide family of CoA transferases. J Biol Chem 2003;278: 34582-6.
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[7] Milosevic D, Rinat C, Batinic D, et al. Genetic analysis--a diagnostic tool for primary hyperoxaluria type I[J]. Pediatr Nephrol, 2002,17(11):896-8.
[8] Pirulli D, Giordano M, Lessi M, et al. Detection of AGXT gene mutations by denaturing high-performance liquid chromatography for diagnosis of hyperoxaluria type 1[J]. Clin Exp Med, 2001,1(2):99-104.
[9] Amoroso A, Pirulli D, Florian F, et al. AGXT gene mutations and their influence on clinical heterogeneity of type 1 primary hyperoxaluria[J]. J Am Soc Nephrol, 2001,12(10):2072-9.
[10] Rumsby G, Williams E, Coulter-Mackie M. Evaluation of mutation screening as a first line test for the diagnosis of the primary hyperoxalurias[J]. Kidney Int, 2004,66(3):959-63.
[11] Williams HE, Smith LH Jr. L-glyceric aciduria. A new genetic variant of primary hyperoxaluria[J]. N Engl J Med, 1968,278(5):233-8.
[12] Cramer SD, Ferree PM, Lin K, et al. The gene encoding hydroxypyruvate reductase (GRHPR) is mutated in patients with primary hyperoxaluria type II[J]. Hum Mol Genet, 1999,8(11):2063-9.
[13] Cregeen DP, Williams EL, Hulton S, et al. Molecular analysis of the glyoxylate reductase (GRHPR) gene and description of mutations underlying primary hyperoxaluria type 2[J]. Hum Mutat, 2003,22(6):497.
[14] Webster KE, Ferree PM, Holmes RP, et al. Identification of missense, nonsense, and deletion mutations in the GRHPR gene in patients with primary hyperoxaluria type II (PH2)[J]. Hum Genet, 2000,107(2):176-85.
[15] Rumsby G. Is liver analysis still required for the diagnosis of primary hyperoxaluria type 2?[J]. Nephrol Dial Transplant, 2006,21(8):2063-4.
[16] Goodman, HO, Holmes, RP, Assimos, DG. Genetic factors in calcium oxalate stone disease[J]. J Urol, 1995,153(2):301-7.
[17] Zhang XX, Rozen R, Hediger MA, et al. Assignment of the gene for cystinuria (SLC3A1) to human chromosome 2p21 by fluorescence in situ hybridization[J]. Genomics, 1994,24(2):413-4.
[18] Feliubadalo L, Font M, Purroy J, et al. Non-type I cystinuria caused by mutations in SLC7A9, encoding a subunit (bo,+AT) of rBAT[J]. Nat Genet, 1999,23(1):52-7.
[19] Skopkova Z, Hrabincova E, Stastna S, et al. Molecular genetic analysis of SLC3A1 and SLC7A9 genes in Czech and Slovak cystinuric patients[J]. Ann Hum Genet, 2005,69(Pt 5):501-7.
[20] Brauers E, Vester U, Zerres K, et al. Search for mutations in SLC1A5 (19q13) in cystinuria patients[J]. J Inherit Metab Dis, 2005,28(6):1169-71.
[21] Anderson WF. Prospects for human gene therapy[J]. Science, 1984,226(4673):401-9.
[22] Blaese RM, Culver KW, Miller AD, et al. T lymphocyte-directed gene therapy for ADA- SCID: initial trial results after 4 years[J]. Science, 1995,270(5235):475-80.
[23] Li LC, Okino ST, Zhao H, et al. Small dsRNAs induce transcriptional activation in human cells[J]. Proc Natl Acad Sci U S A, 2006,103(46):17337-42.
[24] Garber K. Genetics. Small RNAs reveal an activating side[J]. Science, 2006,314(5800):741-2.
[25] Danpure CJ. Advances in the enzymology and molecular genetics of primary hyperoxaluria type 1. Prospects for gene therapy[J]. Nephrol Dial Transplant, 1995,10 Suppl 8:24-9.
[26] Cochat P. Primary hyperoxaluria type 1[J]. Kidney Int, 1999,55(6):2533-47.
[27] Koul S, Johnson T, Pramanik S, et al. Cellular transfection to deliver alanine-glyoxylate aminotransferase to hepatocytes: a rational gene therapy for primary hyperoxaluria-1 (PH-1)[J]. Am J Nephrol, 2005,25(2):176-82.
[28] Cochat P, Basmaison O. Current approaches to the management of primaryhyperoxaluria[J]. Arch Dis Child, 2000,82(6):470-3.
[29] Danpure CJ. Molecular etiology of primary hyperoxaluria type 1: new directions for treatment[J]. Am J Nephrol, 2005,25(3):303-10.
[30] Hoppe B, Beck B, Gatter N, et al. Oxalobacter formigenes: a potential tool for the treatment of primary hyperoxaluria type 1[J]. Kidney Int, 2006.
[31] Hatch M, Cornelius J, Allison M, et al. Oxalobacter sp. reduces urinary oxalate excretion by promoting enteric oxalate secretion[J]. Kidney Int, 2006,69(4):691-8.
[32] Hoppe B, Leumann E. Diagnostic and therapeutic strategies in hyperoxaluria: a plea for early intervention[J]. Nephrol Dial Transplant, 2004,19(1):39-42.
[33] Knoll T, Sagi S, Trojan L, et al. In vitro and ex vivo gene delivery into proximal tubular cells by means of laser energy--a potential approach for curing cystinuria?[J]. Urol Res, 2004,32(2):129-32.
1. James LF: Oxalate toxicosis. Clin Toxicol 5: 231-243, 1972.
2. Leumann E and Hoppe B: The primary hyperoxalurias. J Am Soc Nephrol 12: 1986-1993, 2001.
3. Cornelius JG and Peck AB: Colonization of the neonatal rat intestinal tract from environmental exposure to the anaerobic bacterium Oxalobacter formigenes. J Med Microbiol 53: 249-254, 2004.
4. Kumar R, Mukherjee M, Bhandari M, Kumar A, Sidhu H and Mittal RD: Role of Oxalobacter formigenes in calcium oxalate stone disease: a study from North India. Eur Urol 41: 318-322, 2002.
5. Allison MJ, Dawson KA, Mayberry WR and Foss JG: Oxalobacter formigenes gen. nov., sp. nov.: oxalate-degrading anaerobes that inhabit the gastrointestinal tract. Arch Microbiol 141: 1-7, 1985.
6. Dawson KA, Allison MJ and Hartman PA: Isolation and some characteristics of anaerobic oxalate-degrading bacteria from the rumen. Appl Environ Microbiol 40: 833-839, 1980.
7. Allison MJ and Cook HM: Oxalate degradation by microbes of the large bowel of herbivores: the effect of dietary oxalate. Science 212: 675-676, 1981.
8. Smith RL, Strohmaier FE and Oremland RS: Isolation of anaerobic oxalate-degrading bacteria from freshwater lake sediments. Arch Microbiol 141: 8-13, 1985.
9. Baetz AL and Allison MJ: Purification and characterization of oxalyl-coenzyme A decarboxylase from Oxalobacter formigenes. J Bacteriol 171: 2605-2608, 1989.
10. Baetz AL and Allison MJ: Purification and characterization of formyl-coenzyme A transferase from Oxalobacter formigenes. J Bacteriol 172: 3537-3540, 1990.
11. Ricagno S, Jonsson S, Richards N and Lindqvist Y: Formyl-CoA transferase encloses the CoA binding site at the interface of an interlocked dimer. Embo J 22: 3210-3219,2003.
12. Jonsson S, Ricagno S, Lindqvist Y and Richards NG: Kinetic and mechanistic characterization of the formyl-CoA transferase from Oxalobacter formigenes. J Biol Chem 279: 36003-36012, 2004.
13. Quayle JR: Carbon assimilation by Pseudomonas oxalaticus (OX1). 6. Reactions of oxalyl-coenzyme A. Biochem J 87: 368-373, 1963.
14. Demoz A, Garras A, Asiedu DK, Netteland B and Berge RK: Rapid method for the separation and detection of tissue short-chain coenzyme A esters by reversed-phase high-performance liquid chromatography. J Chromatogr B Biomed Appl 667: 148-152, 1995.
15. Allison MJ, Cook HM, Milne DB, Gallagher S and Clayman RV: Oxalate degradation by gastrointestinal bacteria from humans. J Nutr 116: 455-460, 1986.
16. Duncan SH, Richardson AJ, Kaul P, Holmes RP, Allison MJ and Stewart CS: Oxalobacter formigenes and its potential role in human health. Appl Environ Microbiol 68: 3841-3847, 2002.
17. Sidhu H, Enatska L, Ogden S, Williams WN, Allison MJ and Peck AB: Evaluating Children in the Ukraine for Colonization With the Intestinal Bacterium Oxalobacter formigenes, Using a Polymerase Chain Reaction-based Detection System. Mol Diagn 2: 89-97, 1997.
18. Sidhu H, Schmidt ME, Cornelius JG, et al.: Direct correlation between hyperoxaluria/oxalate stone disease and the absence of the gastrointestinal tract-dwelling bacterium Oxalobacter formigenes: possible prevention by gut recolonization or enzyme replacement therapy. J Am Soc Nephrol 10 Suppl 14: S334-340, 1999.
19. Kwak C, Kim HK, Kim EC, Choi MS and Kim HH: Urinary oxalate levels and the enteric bacterium Oxalobacter formigenes in patients with calcium oxalate urolithiasis. Eur Urol 44: 475-481, 2003.
20. Mittal RD, Kumar R, Mittal B, Prasad R and Bhandari M: Stone composition, metabolic profile and the presence of the gut-inhabiting bacterium Oxalobacter formigenes as risk factors for renal stone formation. Med Princ Pract 12: 208-213, 2003.
21. Mittal RD, Kumar R, Bid HK and Mittal B: Effect of antibiotics on Oxalobacter formigenes colonization of human gastrointestinal tract. J Endourol 19: 102-106, 2005.
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24. Lung HY, Baetz AL and Peck AB: Molecular cloning, DNA sequence, and gene expression of the oxalyl-coenzyme A decarboxylase gene, oxc, from the bacterium Oxalobacter formigenes. J Bacteriol 176: 2468-2472, 1994.
25. Sidhu H, Ogden SD, Lung HY, Luttge BG, Baetz AL and Peck AB: DNA sequencing and expression of the formyl coenzyme A transferase gene, frc, from Oxalobacter formigenes. J Bacteriol 179: 3378-3381, 1997.
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[2] Ricagno S, Jonsson S, Richards N, Lindqvist Y. Formyl-CoA transferase encloses the CoA binding site at the interface of an interlocked dimer. EMBO J 2003;22: 3210-9.
[3] Tiselius HG. Epidemiology and medical management of stone disease. BJU Int 2003;91: 758-67.
[4]叶章群.泌尿系结石研究现况与展望.中华实验外科杂志2005;22: 261-262.
[5]许四虎,程锦泉,周华,张福林.深圳市肾结石的流行病学调查报告.中华泌尿外科杂志1999;20: 655-657.
[6] Tiselius HG. Stone incidence and prevention. Braz J Urol 2000;26: 452-462.
[7] Holmes RP, Assimos DG. Glyoxylate synthesis, and its modulation and influence on oxalate synthesis. J Urol 1998;160: 1617-24.
[8] Jonassen JA, Kohjimoto Y, Scheid CR, Schmidt M. Oxalate toxicity in renal cells. Urol Res 2005;33: 329-39.
[9] Chen Z, Ye Z, Zeng L, Yang W. Clinical investigation on gastric oxalate absorption. Chin Med J (Engl) 2003;116: 1749-1751.
[10] Allison MJ, Dawson KA, Mayberry WR, Foss JG. Oxalobacter formigenes gen. nov., sp. nov.: oxalate-degrading anaerobes that inhabit the gastrointestinal tract. Arch Microbiol 1985;141: 1-7.
[11]陈志强,郭辉,叶章群,朱旭慧,余建华,曾令启.人肠道产甲酸草酸杆菌的分离培养.中华实验外科杂志2005;22: 1402-1403.
[12] Jonsson S, Ricagno S, Lindqvist Y, Richards NG. Kinetic and mechanistic characterization of the formyl-CoA transferase from Oxalobacter formigenes. J Biol Chem 2004;279: 36003-12.
[13] Sly WS, Stadtman ER. Formate metabolism. I. Formyl coenzyme A, an intermediate inthe formate-dependent decomposition of acetyl phosphate in Clostridium kluyveri. J Biol Chem 1963;238: 2632-8.
[14] Mittal RD, Kumar R. Gut-inhabiting bacterium Oxalobacter formigenes: role in calcium oxalate urolithiasis. J Endourol 2004;18: 418-24.
[15] Sidhu H, Allison M, Peck AB. Identification and classification of Oxalobacter formigenes strains by using oligonucleotide probes and primers. J Clin Microbiol 1997;35: 350-3.
[16] Baetz AL, Allison MJ. Purification and characterization of oxalyl-coenzyme A decarboxylase from Oxalobacter formigenes. J Bacteriol 1989;171: 2605-8.
[17] Baetz AL, Allison MJ. Purification and characterization of formyl-coenzyme A transferase from Oxalobacter formigenes. J Bacteriol 1990;172: 3537-40.
[18] Lung HY, Cornelius JG, Peck AB. Cloning and expression of the oxalyl-CoA decarboxylase gene from the bacterium, Oxalobacter formigenes: prospects for gene therapy to control Ca-oxalate kidney stone formation. Am J Kidney Dis 1991;17: 381-5.
[19] Lung HY, Baetz AL, Peck AB. Molecular cloning, DNA sequence, and gene expression of the oxalyl-coenzyme A decarboxylase gene, oxc, from the bacterium Oxalobacter formigenes. J Bacteriol 1994;176: 2468-72.
[20] Sidhu H, Ogden SD, Lung HY, Luttge BG, Baetz AL, Peck AB. DNA sequencing and expression of the formyl coenzyme A transferase gene, frc, from Oxalobacter formigenes. J Bacteriol 1997;179: 3378-81.
[21] Heider J. A new family of CoA-transferases. FEBS Lett 2001;509: 345-9.
[22] Kwak C, Jeong BC, Kim HK, Kim EC, Chox MS, Kim HH. Molecular epidemiology of fecal Oxalobacter formigenes in healthy adults living in Seoul, Korea. J Endourol 2003;17: 239-43.
[1]叶章群.泌尿系结石研究现况与展望.中华实验外科杂志2005;22: 261-262.
[2] Tiselius HG. Stone incidence and prevention. Braz J Urol 2000;26: 452-462.
[3] Chen Z, Ye Z, Zeng L, Yang W. Clinical investigation on gastric oxalate absorption. Chin Med J (Engl) 2003;116: 1749-1751.
[4] Sidhu H, Schmidt ME, Cornelius JG, Thamilselvan S, Khan SR, Hesse A, Peck AB. Direct correlation between hyperoxaluria/oxalate stone disease and the absence of the gastrointestinal tract-dwelling bacterium Oxalobacter formigenes: possible prevention by gut recolonization or enzyme replacement therapy. J Am Soc Nephrol 1999;10 Suppl 14: S334-40.
[5] Allison MJ, Dawson KA, Mayberry WR, Foss JG. Oxalobacter formigenes gen. nov., sp. nov.: oxalate-degrading anaerobes that inhabit the gastrointestinal tract. Arch Microbiol 1985;141: 1-7.
[6]陈志强,郭辉,叶章群,朱旭慧,余建华,曾令启.人肠道产甲酸草酸杆菌的分离培养.中华实验外科杂志2005;22: 1402-1403.
[7] Mittal RD, Kumar R. Gut-inhabiting bacterium Oxalobacter formigenes: role in calcium oxalate urolithiasis. J Endourol 2004;18: 418-24.
[8] Sidhu H, Allison M, Peck AB. Identification and classification of Oxalobacter formigenes strains by using oligonucleotide probes and primers. J Clin Microbiol 1997;35: 350-3.
[9] Baetz AL, Allison MJ. Purification and characterization of oxalyl-coenzyme A decarboxylase from Oxalobacter formigenes. J Bacteriol 1989;171: 2605-8.
[10] Baetz AL, Allison MJ. Purification and characterization of formyl-coenzyme A transferase from Oxalobacter formigenes. J Bacteriol 1990;172: 3537-40.
[11] Lung HY, Cornelius JG, Peck AB. Cloning and expression of the oxalyl-CoA decarboxylase gene from the bacterium, Oxalobacter formigenes: prospects for genetherapy to control Ca-oxalate kidney stone formation. Am J Kidney Dis 1991;17: 381-5.
[12] Lung HY, Baetz AL, Peck AB. Molecular cloning, DNA sequence, and gene expression of the oxalyl-coenzyme A decarboxylase gene, oxc, from the bacterium Oxalobacter formigenes. J Bacteriol 1994;176: 2468-72.
[13] Sidhu H, Ogden SD, Lung HY, Luttge BG, Baetz AL, Peck AB. DNA sequencing and expression of the formyl coenzyme A transferase gene, frc, from Oxalobacter formigenes. J Bacteriol 1997;179: 3378-81.
[14] Azcarate-Peril MA, Bruno-Barcena JM, Hassan HM, Klaenhammer TR. Transcriptional and functional analysis of oxalyl-coenzyme A (CoA) decarboxylase and formyl-CoA transferase genes from Lactobacillus acidophilus. Appl Environ Microbiol 2006;72: 1891-9.
[15] Kwak C, Jeong BC, Kim HK, Kim EC, Chox MS, Kim HH. Molecular epidemiology of fecal Oxalobacter formigenes in healthy adults living in Seoul, Korea. J Endourol 2003;17: 239-43.
[16] Gruez A, Roig-Zamboni V, Valencia C, Campanacci V, Cambillau C. The crystal structure of the Escherichia coli YfdW gene product reveals a new fold of two interlaced rings identifying a wide family of CoA transferases. J Biol Chem 2003;278: 34582-6.
[1]叶章群.泌尿系结石研究现况与展望[J].中华实验外科杂志, 2005,22(3): 261-262.
[2] Saiki RK, Scharf S, Faloona F, et al. Enzymatic amplification of beta-globin genomic sequences and restriction site analysis for diagnosis of sickle cell anemia[J]. Science, 1985,230(4732):1350-4.
[3] Tempfer CB, Riener EK, Hefler LA, et al. DNA microarray-based analysis of single nucleotide polymorphisms may be useful for assessing the risks and benefits of hormone therapy[J]. Fertil Steril, 2004,82(1):132-7.
[4] Noguchi T, Takada Y. Peroxisomal localization of alanine: glyoxylate aminotransferase in human liver[J]. Arch Biochem Biophys, 1979,196(2):645-7.
[5] Cochat P, Gaulier JM, Koch Nogueira PC, et al. Combined liver-kidney transplantation in primary hyperoxaluria type 1[J]. Eur J Pediatr, 1999,158 Suppl2:S75-80.
[6] Pirulli, D, Marangella, M, Amoroso, A. Primary hyperoxaluria: genotype-phenotype correlation[J]. J Nephrol, 2003,16(2):297-309.
[7] Milosevic D, Rinat C, Batinic D, et al. Genetic analysis--a diagnostic tool for primary hyperoxaluria type I[J]. Pediatr Nephrol, 2002,17(11):896-8.
[8] Pirulli D, Giordano M, Lessi M, et al. Detection of AGXT gene mutations by denaturing high-performance liquid chromatography for diagnosis of hyperoxaluria type 1[J]. Clin Exp Med, 2001,1(2):99-104.
[9] Amoroso A, Pirulli D, Florian F, et al. AGXT gene mutations and their influence on clinical heterogeneity of type 1 primary hyperoxaluria[J]. J Am Soc Nephrol, 2001,12(10):2072-9.
[10] Rumsby G, Williams E, Coulter-Mackie M. Evaluation of mutation screening as a first line test for the diagnosis of the primary hyperoxalurias[J]. Kidney Int, 2004,66(3):959-63.
[11] Williams HE, Smith LH Jr. L-glyceric aciduria. A new genetic variant of primary hyperoxaluria[J]. N Engl J Med, 1968,278(5):233-8.
[12] Cramer SD, Ferree PM, Lin K, et al. The gene encoding hydroxypyruvate reductase (GRHPR) is mutated in patients with primary hyperoxaluria type II[J]. Hum Mol Genet, 1999,8(11):2063-9.
[13] Cregeen DP, Williams EL, Hulton S, et al. Molecular analysis of the glyoxylate reductase (GRHPR) gene and description of mutations underlying primary hyperoxaluria type 2[J]. Hum Mutat, 2003,22(6):497.
[14] Webster KE, Ferree PM, Holmes RP, et al. Identification of missense, nonsense, and deletion mutations in the GRHPR gene in patients with primary hyperoxaluria type II (PH2)[J]. Hum Genet, 2000,107(2):176-85.
[15] Rumsby G. Is liver analysis still required for the diagnosis of primary hyperoxaluria type 2?[J]. Nephrol Dial Transplant, 2006,21(8):2063-4.
[16] Goodman, HO, Holmes, RP, Assimos, DG. Genetic factors in calcium oxalate stone disease[J]. J Urol, 1995,153(2):301-7.
[17] Zhang XX, Rozen R, Hediger MA, et al. Assignment of the gene for cystinuria (SLC3A1) to human chromosome 2p21 by fluorescence in situ hybridization[J]. Genomics, 1994,24(2):413-4.
[18] Feliubadalo L, Font M, Purroy J, et al. Non-type I cystinuria caused by mutations in SLC7A9, encoding a subunit (bo,+AT) of rBAT[J]. Nat Genet, 1999,23(1):52-7.
[19] Skopkova Z, Hrabincova E, Stastna S, et al. Molecular genetic analysis of SLC3A1 and SLC7A9 genes in Czech and Slovak cystinuric patients[J]. Ann Hum Genet, 2005,69(Pt 5):501-7.
[20] Brauers E, Vester U, Zerres K, et al. Search for mutations in SLC1A5 (19q13) in cystinuria patients[J]. J Inherit Metab Dis, 2005,28(6):1169-71.
[21] Anderson WF. Prospects for human gene therapy[J]. Science, 1984,226(4673):401-9.
[22] Blaese RM, Culver KW, Miller AD, et al. T lymphocyte-directed gene therapy for ADA- SCID: initial trial results after 4 years[J]. Science, 1995,270(5235):475-80.
[23] Li LC, Okino ST, Zhao H, et al. Small dsRNAs induce transcriptional activation in human cells[J]. Proc Natl Acad Sci U S A, 2006,103(46):17337-42.
[24] Garber K. Genetics. Small RNAs reveal an activating side[J]. Science, 2006,314(5800):741-2.
[25] Danpure CJ. Advances in the enzymology and molecular genetics of primary hyperoxaluria type 1. Prospects for gene therapy[J]. Nephrol Dial Transplant, 1995,10 Suppl 8:24-9.
[26] Cochat P. Primary hyperoxaluria type 1[J]. Kidney Int, 1999,55(6):2533-47.
[27] Koul S, Johnson T, Pramanik S, et al. Cellular transfection to deliver alanine-glyoxylate aminotransferase to hepatocytes: a rational gene therapy for primary hyperoxaluria-1 (PH-1)[J]. Am J Nephrol, 2005,25(2):176-82.
[28] Cochat P, Basmaison O. Current approaches to the management of primaryhyperoxaluria[J]. Arch Dis Child, 2000,82(6):470-3.
[29] Danpure CJ. Molecular etiology of primary hyperoxaluria type 1: new directions for treatment[J]. Am J Nephrol, 2005,25(3):303-10.
[30] Hoppe B, Beck B, Gatter N, et al. Oxalobacter formigenes: a potential tool for the treatment of primary hyperoxaluria type 1[J]. Kidney Int, 2006.
[31] Hatch M, Cornelius J, Allison M, et al. Oxalobacter sp. reduces urinary oxalate excretion by promoting enteric oxalate secretion[J]. Kidney Int, 2006,69(4):691-8.
[32] Hoppe B, Leumann E. Diagnostic and therapeutic strategies in hyperoxaluria: a plea for early intervention[J]. Nephrol Dial Transplant, 2004,19(1):39-42.
[33] Knoll T, Sagi S, Trojan L, et al. In vitro and ex vivo gene delivery into proximal tubular cells by means of laser energy--a potential approach for curing cystinuria?[J]. Urol Res, 2004,32(2):129-32.
1. James LF: Oxalate toxicosis. Clin Toxicol 5: 231-243, 1972.
2. Leumann E and Hoppe B: The primary hyperoxalurias. J Am Soc Nephrol 12: 1986-1993, 2001.
3. Cornelius JG and Peck AB: Colonization of the neonatal rat intestinal tract from environmental exposure to the anaerobic bacterium Oxalobacter formigenes. J Med Microbiol 53: 249-254, 2004.
4. Kumar R, Mukherjee M, Bhandari M, Kumar A, Sidhu H and Mittal RD: Role of Oxalobacter formigenes in calcium oxalate stone disease: a study from North India. Eur Urol 41: 318-322, 2002.
5. Allison MJ, Dawson KA, Mayberry WR and Foss JG: Oxalobacter formigenes gen. nov., sp. nov.: oxalate-degrading anaerobes that inhabit the gastrointestinal tract. Arch Microbiol 141: 1-7, 1985.
6. Dawson KA, Allison MJ and Hartman PA: Isolation and some characteristics of anaerobic oxalate-degrading bacteria from the rumen. Appl Environ Microbiol 40: 833-839, 1980.
7. Allison MJ and Cook HM: Oxalate degradation by microbes of the large bowel of herbivores: the effect of dietary oxalate. Science 212: 675-676, 1981.
8. Smith RL, Strohmaier FE and Oremland RS: Isolation of anaerobic oxalate-degrading bacteria from freshwater lake sediments. Arch Microbiol 141: 8-13, 1985.
9. Baetz AL and Allison MJ: Purification and characterization of oxalyl-coenzyme A decarboxylase from Oxalobacter formigenes. J Bacteriol 171: 2605-2608, 1989.
10. Baetz AL and Allison MJ: Purification and characterization of formyl-coenzyme A transferase from Oxalobacter formigenes. J Bacteriol 172: 3537-3540, 1990.
11. Ricagno S, Jonsson S, Richards N and Lindqvist Y: Formyl-CoA transferase encloses the CoA binding site at the interface of an interlocked dimer. Embo J 22: 3210-3219,2003.
12. Jonsson S, Ricagno S, Lindqvist Y and Richards NG: Kinetic and mechanistic characterization of the formyl-CoA transferase from Oxalobacter formigenes. J Biol Chem 279: 36003-36012, 2004.
13. Quayle JR: Carbon assimilation by Pseudomonas oxalaticus (OX1). 6. Reactions of oxalyl-coenzyme A. Biochem J 87: 368-373, 1963.
14. Demoz A, Garras A, Asiedu DK, Netteland B and Berge RK: Rapid method for the separation and detection of tissue short-chain coenzyme A esters by reversed-phase high-performance liquid chromatography. J Chromatogr B Biomed Appl 667: 148-152, 1995.
15. Allison MJ, Cook HM, Milne DB, Gallagher S and Clayman RV: Oxalate degradation by gastrointestinal bacteria from humans. J Nutr 116: 455-460, 1986.
16. Duncan SH, Richardson AJ, Kaul P, Holmes RP, Allison MJ and Stewart CS: Oxalobacter formigenes and its potential role in human health. Appl Environ Microbiol 68: 3841-3847, 2002.
17. Sidhu H, Enatska L, Ogden S, Williams WN, Allison MJ and Peck AB: Evaluating Children in the Ukraine for Colonization With the Intestinal Bacterium Oxalobacter formigenes, Using a Polymerase Chain Reaction-based Detection System. Mol Diagn 2: 89-97, 1997.
18. Sidhu H, Schmidt ME, Cornelius JG, et al.: Direct correlation between hyperoxaluria/oxalate stone disease and the absence of the gastrointestinal tract-dwelling bacterium Oxalobacter formigenes: possible prevention by gut recolonization or enzyme replacement therapy. J Am Soc Nephrol 10 Suppl 14: S334-340, 1999.
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