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SREE CHITHRA TIRUNAL INSTITUTE FOR MEDICAL SCIENCES TECHNOLOGY

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11. RONAGHJ, M eta/., ( 1996) Real-time DNA sequencing using detection ofpyrophosphate release. Anal Biochem 242:84-89.12. SAKTHIVEL S, VOSBERG H-P, RAJAMANICKAM C. Oligonucleotide ligationassay for rapid and sensitive identification of carriers of a missense mutation in thecardiac B-myosin heavy chain gene causing hypertrophic cardiomyopathy in an Indianfamily. Current Science 2000; 12(80): 1588-1592.13. EPSTEIN NO, COHN GM, CYRAN F, FANANAPAZIR L. Differences in clinicalexpression of hypertriophic cardiomyopathy associated with two distinct mutations in theU-myosin heavy chain gene. A 908 Leu-Val mutation and a 403 Arg-Gin mutation.Circulation 1992; 86: 345-352.14. WATKINS H, ROSENZWEIG A, HWANG DS, LEVIT, MCKENNA W,SEIDMAN CE, SEIDMAN JG. Characteristics and prognostic implications of myosinmissense mutations in familial hypertrophic cardiomyopathy. N Eng! J Med 1992; 32!-i:1108-1114.t 5. WATKINS H, ROSENZWEIG A, HWANG DS, LEVI T, MCKENNA W,SEIDMAN CE, SEIDMAN JG. Characteristics and prognostic implications of myosinmissense mutations in familial hypertrophic cardiomyopathy [see comments]. N Engl.!Med 1992; 326: 1108-14.16. NISHI H, KIMURA A, HARADA H, ADACHI K, KOGA Y, SASAZUKI T,TSHIMA H. Possible gene dose effect of a mutant cardiac B-myosin heavy chain gene onthe clinical expression of familial hypertrophic cardiomyopathy. Biochem Biophys ResCommun 1994; 200: 549-556.17. RIMM DL, SINARD JH, POLLARD TD. Location of the head-tail junction ofmyosin. J Cell Bioi 1989; 108: 1783-9.18. RAYMENT l, HOLDEN HM, SELLERS JR, FANANAPAZIR L, EPSTEIN NO.Structural interpretation of the mutations in the B-cardiac myosin that have beenimplicated in familial hypertrophic cardiomyopathy. Proc Nat/ Acad Sci USA 1995; 92:3864-3868.19. KNIGHT P J. Dynamic behaviour of the head-tail junction of myosin. J Mol Bioi1996; 255: 269-74.20. CARRIER L, BONNE G, BAHREND E, ET AL. Organization and sequence ofhuman cardiac myosin binding protein C gene (MYBPC3) and identification of mutationspredicted to produce truncated proteins in familial hypertrophic cardiomyopathy.Circulation Res 1997; 80: 427-434.21. RICHARD P, CHARRON P, CHRISTOPHEL, LECLERCQ C, LEDEUIL C,CARRIER L, DUBOURG 0, DESNOS M, BOUHOUR J-B, SCHWARTZ K,DAUBERT C, KOMAJDA M, HAINQUE B. Homozygotes for a R869G mutation in the43

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