scholarly journals Evidence for Linkage Between Essential Hypertension and a Putative Locus on Human Chromosome 17

Hypertension ◽  
1999 ◽  
Vol 34 (1) ◽  
pp. 4-7 ◽  
Author(s):  
Jader Baima ◽  
Michael Nicolaou ◽  
Faina Schwartz ◽  
Anita L. DeStefano ◽  
Athanasios Manolis ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Human Chromosome ◽  
Chromosome 17 ◽  
Human Chromosome 17 ◽  
Putative Locus

Human Chromosome 17 in Essential Hypertension

2003 ◽  
Vol 67 (2) ◽  
pp. 193-206 ◽  
Author(s):  
J. Knight ◽  
P. B. Munroe ◽  
J. C. Pembroke ◽  
M. J. Caulfield
Keyword(s):  
Essential Hypertension ◽  
Human Chromosome ◽  
Chromosome 17 ◽  
Human Chromosome 17

The Gene Encoding Protein Kinase SEK1 Maps to Mouse Chromosome 11 and Human Chromosome 17

Genomics ◽  
1996 ◽  
Vol 34 (3) ◽  
pp. 430-432 ◽  
Author(s):  
Robert A. White ◽  
Rowland T. Hughes ◽  
Linda R. Adkison ◽  
Gail Bruns ◽  
Leonard I. Zon
Keyword(s):  
Protein Kinase ◽  
Human Chromosome ◽  
Mouse Chromosome ◽  
Chromosome 17 ◽  
Chromosome 11 ◽  
Gene Encoding ◽  
Human Chromosome 17 ◽  
Mouse Chromosome 11 ◽  
Encoding Protein

scholarly journals Mapping blood pressure loci in (A/J × B6)F2 mice

2003 ◽  
Vol 15 (3) ◽  
pp. 236-242 ◽  
Author(s):  
David D. L. Woo ◽  
Ira Kurtz
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Environmental Variables ◽  
Chromosome 17 ◽  
Whole Genome ◽  
Lod Score ◽  
Human Hypertension ◽  
Complex Genetics ◽  
The Common ◽  
Human Chromosome 17

Although the genetics of rare, monogenic, forms of human hypertension are fairly well defined, the genetics of the common polygenic form of human essential hypertension is only emerging. With the ability to control environmental variables, animal models have provided valuable tools with which to study blood pressure (BP) homeostasis. We have now studied BP genetics in a model consisting of 1,521 F2 mice from a series of (A/J × B6) intercrosses kept under standardized conditions. Using whole genome quantitative trait loci (QTL) mapping, we have identified four novel significant BP loci. These included Abbp1 on mouse chromosome MMU1 [maximum LOD score (MLS) at ∼35 cM = 6.8], Abbp2 on MMU4 (MLS at ∼25 cM = 9.8), Abbp3 on MMU7 (MLS at ∼25 cM = 5.4), and Abbp4 on MMU11 (MLS at ∼58 cM = 6.3). Compared with A/J homozygotes, homozygosity for the B6 alleles of Abbp1, Abbp2, or Abbp4 is independently associated with a 7–12 mmHg increase in BP. In contrast Abbp3 interacts epistatically with a locus on MMU17 (near D17Mit180) to modulate BPs in female (A/J × B6)F2 mice. Interestingly, Abbp4 on MMU11 is homologous to a major confirmed BP locus, BP1, on rat chromosome 10 and to a major confirmed BP locus, HYT1, on human chromosome 17. Defining the molecular differences between the A/J and the B6 alleles at these novel loci with major influences on the BP phenotype will contribute to our understanding of the complex genetics of BP control.

Nucleotide sequence of the third cytokine LD78 gene and mapping of all three LD78 gene loci to human chromosome 17

DNA Sequence ◽  
1992 ◽  
Vol 3 (4) ◽  
pp. 203-212 ◽  
Author(s):  
M. Hirashima ◽  
T. Ono ◽  
M. Nakao ◽  
H. Nishi ◽  
A. Kimura ◽  
...  
Keyword(s):  
Nucleotide Sequence ◽  
Human Chromosome ◽  
Chromosome 17 ◽  
The Third ◽  
Human Chromosome 17

Glial fibrillary acid protein, an astrocytic-specific marker, maps to human chromosome 17

Genomics ◽  
1991 ◽  
Vol 10 (4) ◽  
pp. 1087-1089 ◽  
Author(s):  
Elise Brownell ◽  
Alice S. Lee ◽  
Susan K. Pekar ◽  
Dimitrina Pravtcheva ◽  
Frank H. Ruddle ◽  
...  
Keyword(s):  
Human Chromosome ◽  
Chromosome 17 ◽  
Glial Fibrillary Acid Protein ◽  
Specific Marker ◽  
Acid Protein ◽  
Human Chromosome 17

scholarly journals Partial deletion of alpha satellite DNA associated with reduced amounts of the centromere protein CENP-B in a mitotically stable human chromosome rearrangement.

1990 ◽  
Vol 10 (12) ◽  
pp. 6374-6380 ◽  
Author(s):  
R Wevrick ◽  
W C Earnshaw ◽  
P N Howard-Peebles ◽  
H F Willard
Keyword(s):  
Human Chromosome ◽  
Satellite Dna ◽  
Centromeric Region ◽  
Chromosome Rearrangement ◽  
Specific Antigen ◽  
Chromosome 17 ◽  
Alpha Satellite ◽  
Protein Antigens ◽  
Alpha Satellite Dna ◽  
Human Chromosome 17

A familial, constitutionally rearranged human chromosome 17 is deleted for much of the DNA in its centromeric region but retains full mitotic centromere activity. Fluorescence in situ hybridization, pulsed-field gel electrophoresis, and Southern blot analysis of the residual centromeric region revealed a approximately 700-kb centromeric array of tandemly repeated alpha satellite DNA that was only approximately 20 to 30% as large as a normal array. This deletion was associated with a reduction in the amount of the centromere-specific antigen CENP-B detected by indirect immunofluorescence. The coincidence of the primary constriction, the small residual array of alpha satellite DNA, and the reduced amount of detectable CENP-B support the hypothesis that CENP-B is associated with alpha satellite DNA. Furthermore, the finding that both the deleted chromosome 17 and its derivative supernumerary fragment retained mitotic function and possess centromeric protein antigens suggests that human centromeres are structurally and functionally repetitive.

scholarly journals Amplification of the neu (c-erbB-2) oncogene in human mammmary tumors is relatively frequent and is often accompanied by amplification of the linked c-erbA oncogene.

1987 ◽  
Vol 7 (5) ◽  
pp. 2019-2023 ◽  
Author(s):  
M van de Vijver ◽  
R van de Bersselaar ◽  
P Devilee ◽  
C Cornelisse ◽  
J Peterse ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Chromosome ◽  
High Frequency ◽  
Human Breast Cancer ◽  
Functional Role ◽  
Chromosome 17 ◽  
Human Breast ◽  
Copy Numbers ◽  
Neu Oncogene ◽  
Human Chromosome 17

We investigated alterations in the structure and expression of oncogenes in mammary tumors and mammary tumor-derived cell lines. In 16 of 95 samples, we detected amplification of the human neu oncogene, also known as c-erB-2, accompanied by overexpression in the tumors from which intact RNA could be isolated. In 10 of these DNAs, the linked oncogene c-erbA was also amplified, whereas another gene on human chromosome 17, p53, was present in normal copy numbers. Overexpression of c-erbA could not be detected in the tumors analyzed. The relatively high frequency of neu amplification points to a functional role in human breast cancer. Coamplification of the c-erbA oncogene could contribute to this disease as well but is most likely fortuitous.

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