Abstract: A method of treating an injury to hyaline cartilage in a subject in need thereof. The method comprises administering to the subject a therapeutically effective amount of amelogenin.

Abstract: A method of promoting nerve growth or regeneration in a subject in need thereof, wherein the subject is not afflicted with a substantial connective tissue damage, is provided. The method comprises administering to the subject a therapeutically effective amount of full-length amelogenin, thereby promoting nerve growth or regeneration in the subject.

Abstract: A method of promoting nerve growth or regeneration in a subject in need thereof, wherein the subject is not afflicted with a substantial connective tissue damage, is provided. The method comprises administering to the subject a therapeutically effective amount of full-length amelogenin, thereby promoting nerve growth or regeneration in the subject.

Abstract: A method of treating an injury to hyaline cartilage in a subject in need thereof. The method comprises administering to the subject a therapeutically effective amount of amelogenin.

Abstract: A method of treating an injury to hyaline cartilage in a subject in need thereof. The method comprises administering to the subject a therapeutically effective amount of amelogenin.

Abstract: A method of treating an injury to hyaline cartilage in a subject in need thereof. The method comprises administering to the subject a therapeutically effective amount of amelogenin.

Abstract: A method of treating an injury to or a disease of a skeletal joint ligament is disclosed. The method comprises contacting the skeletal joint ligament or tendon of the subject with a therapeutically effective amount of amelogenin, wherein the amelogenin is not comprised in a scaffold, thereby treating the injury to or disease of the skeletal joint ligament or tendon.

Abstract: Familial dysautonomia (FD), the Riley-Day syndrome, is an autosomal recessive disorder characterized by developmental loss of neurons from the sensory and autonomic nervous system. It is limited to the Ashkenazi Jewish population, where the carrier frequency is 1 in 30. We have mapped the FD gene to the chromosome region 9q31-q33 by linkage with ten DNA markers in twenty-six families. The maximum lod score of 21.1 with no recombinants was achieved with D9S58. This marker also showed strong linkage disequilibrium with FD, with one allele present on 73% of all affected chromosomes compared to 5.4% of control chromosomes (X2=3142, 15 d.f. p<0.0001). The other nine markers, distributed within 23 cM proximal or distal to D9S58, also yielded significant linkage to FD. D9S53 and D9S105 represent the closest flanking markers for the disease gene. This localization will permit prenatal diagnosis of FD in affected families.

Abstract: Familial dysautonomia (FD), the Riley-Day syndrome, is an autosomal recessive disorder characterized by developmental loss of neurons from the sensory and autonomic nervous system. It is limited to the Ashkenazi Jewish population, where the carrier frequency is 1 in 30. We have mapped the FD gene to the chromosome region 9q31-q33 by linkage with ten DNA markers in twenty-six families. The maximum lod score of 21.1 with no recombinants was achieved with D9S58. This marker also showed strong linkage disequilibrium with FD, with one allele present on 73% of all affected chromosomes compared to 5.4% of control chromosomes (X2=3142, 15 d.f. p<0.0001). The other nine markers, distributed within 23 cM proximal or distal to D9S58, also yielded significant linkage to FD. D9S53 and D9S105 represent the closest flanking markers for the disease gene. This localization will permit prenatal diagnosis of FD in affected families.

Abstract: Familial dysautonomia (FD), the Riley-Day syndrome, is an autosomal recessive disorder characterized by developmental loss of neurons from the sensory and autonomic nervous system. It is limited to the Ashkenazi Jewish population, where the carrier frequency is 1 in 30. We have mapped the FD gene to the chromosome region 9q31-q33 by linkage with ten DNA markers in twenty-six families. The maximum lod score of 21.1 with no recombinants was achieved with D9S58. This marker also showed strong linkage disequilibrium with FD, with one allele present on 73% of all affected chromosomes compared to 5.4% of control chromosomes (X2=3142, 15 d.f. p<0.0001). The other nine markers, distributed within 23 cM proximal or distal to D9S58, also yielded significant linkage to FD. D9S53 and D9S105 represent the closest flanking markers for the disease gene. This localization will permit prenatal diagnosis of FD in affected families.

Abstract: Familial dysautonomia (FD), the Riley-Day syndrome, is an autosomal recessive disorder characterized by developmental loss of neurons from the sensory and autonomic nervous system. It is limited to the Ashkenazi Jewish population, where the carrier frequency is 1 in 30. We have mapped the FD gene to the chromosome region 9q31-q33 by linkage with ten DNA markers in twenty-six families. The maximum lod score of 21.1 with no recombinants was achieved with D9S58. This marker also showed strong linkage disequilibrium with FD, with one allele present on 73% of all affected chromosomes compared to 5.4% of control chromosomes (X.sup.2 =3142, 15 d.f. p<0.0001). The other nine markers, distributed within 23 cM proximal or distal to D9S58, also yielded significant linkage to FD. D9S53 and D9S105 represent the closest flanking markers for the disease gene. This localization will permit prenatal diagnosis of FD in affected families.

Abstract: The familial dysautonomia gene is identified as located on the long arm of human chromosome 9. As a result of this localization, the presence of the familial dysautonomia gene in a subject of a family with an affected individual is detected by analyzing human chromosome 9 of the subject for a DNA sequence containing the familial dysautonomia gene on the long arm of human chromosome 9 located between D9S59 and D9S127.