Report of the committee on the genetic constitution of chromosomes 18, 19, 20, 21, and 22

Westerveld, A.; Naylor, S.

doi:10.1159/000132008

Cited by 27 publications

(12 citation statements)

References 18 publications

(20 reference statements)

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“…5 Lower). Isozyme data on this clone we with this finding, being positive only for the ge oxide dismutase (soluble), SOD], located on ch at q21.1 (36). The (27).…”

Section: Methodssupporting

confidence: 57%

A human c-erbA oncogene homologue is closely proximal to the chromosome 17 breakpoint in acute promyelocytic leukemia.

Dayton¹,

Selden²,

Laws³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

104

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A human c-erbA oncogene homologue is closely proximal to the chromosome 17 breakpoint in acute promyelocytic leukemia (somatic cell Contributed by Peter C. Nowell, April 5, 1984 ABSTRACT A human cDNA library was screened for sequences homologous to the erbA gene of avian erythroblastosis virus (AEV). One such clone, cHerbA-1, was used to map the chromosomal location of highly homologous human sequences that were found to be present on chromosome 17 as judged by Southern blot screening of a panel of mouse-human hybrid cell lines segregating human chromosomes. cHerbA-1 was hybridized in situ to metaphase chromosomes from a normal male subject and from a female patient with an acute promyelocytic leukemia (APL) having the typical t(15;17) translocation. The results localized the cellular c-erbA sequences on chromosome 17 to the q21-q24 region of normal chromosomes and indicated that the c-erbA sequences remained on the 17q-chromosome in the APL cells, suggesting that they could be assigned to the 17(q21-q22) region. For additional data, we hybridized human neoplastic cells derived from a poorly differentiated acute leukemia carrying a t(17;21) translocation with thymidine kinase (TK)-deficient LMTK-mouse cells. A resulting hybrid, containing only the 21q+ chromosome, did not have human c-erbA sequences. Since the breakpoint on 17q in this translocation was similar to that in the APL t(15;17) translocation, this supported the assignment of c-erbA to the q21-q22 region of chromosome 17. The apparent close proximity of the c-erbA sequences to the chromosomal breakpoints in these two leukemias suggests a possible role for this oncogene homologue in the development of these neoplasms.

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“…5 Lower). Isozyme data on this clone we with this finding, being positive only for the ge oxide dismutase (soluble), SOD], located on ch at q21.1 (36). The (27).…”

Section: Methodssupporting

confidence: 57%

A human c-erbA oncogene homologue is closely proximal to the chromosome 17 breakpoint in acute promyelocytic leukemia.

Dayton¹,

Selden²,

Laws³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

104

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“…We have only been able to find one reference (Smith et al 1983) to a linkage between a simple marker and a disease that does not have a known mendelian basis that has been established in the absence of a previously known population association between the disease and the marker. On the other hand, rare diseases with a mendelian aetiology are being located: for example, an allele involved in classical neurofibromatosis is now thought to be on chromosome 19 (Westerveld & Naylor, 1984).…”

Section: The Future?mentioning

confidence: 99%

Can linkage and marker association resolve the genetic aetiology of psychiatric disorders? Review and argument

Sturt¹,

McGuffin²

1985

Psychol. Med.

103

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“…Human chromosome 19 contains genes involved in several familial diseases and, hence, has become a focus for genetic studies (1)(2)(3). Among these are genes for myotonic dystrophy (DM) and a form of neurofibromatosis (NFI) and several genes controlling lipoprotein structure and metabolism (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12).…”

mentioning

confidence: 99%

“…Among these are genes for myotonic dystrophy (DM) and a form of neurofibromatosis (NFI) and several genes controlling lipoprotein structure and metabolism (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Considering its small size, chromosome 19 has been assigned a large number of other genes, including complement component 3 (C3), peptidase D (PEPD), glucose phosphate isomerase (GPI), secretor (SE), the Lutheran blood group (LU), and a cluster of genes related to chorionic gonadotropin p subunit (CGB) (1,13). However, the regional locations of these genes have been poorly defined.…”

mentioning

confidence: 99%

Regional mapping of human chromosome 19: organization of genes for plasma lipid transport (APOC1, -C2, and -E and LDLR) and the genes C3, PEPD, and GPI.

Lusis¹,

Heinzmann²,

Sparkes³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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We report the regional mapping of human chromosome 19 genes for three apolipoproteins and a lipoprotein receptor as well as genes for three other markers. The regional mapping was made possible by the use of a reciprocal whole-arm translocation between the long arm of chromosome 19 and the short arm of chromosome 1. Examination of three separate somatic cell hybrids containing the long arm but not the short arm of chromosome 19 indicated that the genes for apolipoproteins CI, CII, and E (APOCI, APOC2, and APOE, respectively) and glucose-6-phosphate isomerase (GPI) reside on the long arm, whereas genes for the low density lipoprotein receptor (LDLR), complement component 3 (C3), and peptidase D (PEPD) reside on the short arm. When taken together with previous studies, our results suggest the following physical gene map: pter-LDLR-C3-pl3.2-PEPD-centromere-(APOE, APOCI, APOC2, GPI)-qter. In addition, we have isolated a single A phage carrying both APOCI and part ofAPOE. These genes are tandemly oriented and are separated by about 6 kilobases of genomic DNA. Since previous family studies indicate tight linkage of APOE and APOC2, the apolipoprotein genes APOCI, APOC2, and APOE form a tight complex on the long arm of chromosome 19, suggesting the possibility of coordinate regulation.

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Report of the committee on the genetic constitution of chromosomes 18, 19, 20, 21, and 22

Cited by 27 publications

References 18 publications

A human c-erbA oncogene homologue is closely proximal to the chromosome 17 breakpoint in acute promyelocytic leukemia.

A human c-erbA oncogene homologue is closely proximal to the chromosome 17 breakpoint in acute promyelocytic leukemia.

Can linkage and marker association resolve the genetic aetiology of psychiatric disorders? Review and argument

Regional mapping of human chromosome 19: organization of genes for plasma lipid transport (APOC1, -C2, and -E and LDLR) and the genes C3, PEPD, and GPI.

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