Disease relevance of Edpm9

• Homozygous deletions on the short arm of chromosome 9 in ovarian adenocarcinoma cell lines and loss of heterozygosity in sporadic tumors [1].
• Genome-wide linkage analysis of chronic relapsing experimental autoimmune encephalomyelitis in the rat identifies a major susceptibility locus on chromosome 9 [2].
• Multifocal renal cell carcinoma in sibs from a chromosome 9 linked (TSC1) tuberous sclerosis family [3].
• Neither chromosome 7, previously reported to bear some of the genes controlling metastasis in human X mouse T-cell hybrids, nor chromosome 9 appeared to be correlated with the metastatic potential of LF X ICIG hybrids [4].
• A congenic strain introgressing the R low-blood-pressure QTL allele on chromosome 9 into the S strain was constructed [5].

High impact information on Edpm9

• The loci define 21 large linkage groups corresponding to the 21 rat chromosomes, together with a pair of nearby markers on chromosome 9 that are not linked to the rest of the map [6].
• Translocations involving the abl locus on chromosome 9 fuses the tyrosine kinase c-ABL to proteins harboring oligomerization interfaces such as BCR or TEL, enabling these ABL-fusion proteins (X-ABL) to transform cells and to induce leukemia [7].
• Studies of congenic lines in the Brown Norway rat model of Th2-mediated immunopathological disorders show that the aurothiopropanol sulfonate-induced immunological disorder (Aiid3) locus on chromosome 9 plays a major role compared to Aiid2 on chromosome 10 [8].
• Genome scanning identified one quantitative trait locus on chromosome 9 (approximately 17 centiMorgan (cM); log of the odds ratio (LOD) score 3.9) [9].
• A new QTL, Ciaa3, associating with anticollagen antibody titer (antibody to PII LOD 6.5; antibody to rat type II collagen LOD 5.2) mapped to chromosome 9 [10].

Biological context of Edpm9

• It is located on chromosome 9 within 5.3 centimorgans of the phosphoglucomutase-3 locus and is closely linked (within 3.0 centimorgans) to the gene specifying a highly homologous intracellular retinol binding protein known as CRBP [11].
• The new interval, Atps3, identified on chromosome 9 (Lod score = 16), appears to play a major role in the control of the IgE response since it accounts for 31% of the genetic variance [12].
• Canine tricuspid valve malformation (CTVM) maps to canine chromosome 9 (CFA9), in a region syntenic with gene-dense human chromosome 17q [13].
• A blood pressure (BP) quantitative trait locus (QTL) was previously found on rat chromosome 9 using Dahl salt-sensitive (S) and Dahl salt-resistant (R) rats [14].
• Chromosome 9 and the X chromosome appeared to have an enhanced susceptibility of alterations [15].

Anatomical context of Edpm9

• The locus could be provisionally assigned either to chromosome 9 or to chromosome 10 by correlating the presence or absence of mouse-specific DNA fragments reactive with the probe in a panel of somatic hybrid cell lines with the presence or absence of the various mouse chromosomes [16].

Associations of Edpm9 with chemical compounds

• The mouse RALDH2 gene spans >50 kb, has a structure similar to that of human class 1 aldehyde dehydrogenase genes, and localizes to the central region of chromosome 9 by single-strand polymorphism analysis [17].
• Assignment of the mouse tartrate-resistant acid phosphatase gene (Acp5) to chromosome 9 [18].

Other interactions of Edpm9

• We also find evidence for interaction (epistasis) between Edpm3 and Edpm9 and between Edpm5 and the suggested QTL on Chr 14 [19].
• This area of chromosome 9 also contains a short, direct tandem repeat in close proximity to a paternally methylated NotI site 30 kb upstream of Rasgrf1 [20].
• Comparative mapping between human and rat indicated that the Nidd8/of genomic region, near D9rat21 on rat chromosome 9, contains the calpain10 (Capn10) gene, which is putative type 2 diabetes-susceptibility gene in humans [21].
• Radiation hybrid mapping, using two separate PCR amplicons from rat alpha3(IV)NC1, localized rat Col4a3 to a region of chromosome 9 [22].
• Our findings indicated that epithelial hyperplasia of the choledocho-pancreatic duct is associated with a region on rat chromosome 14 around the Cckar gene in an additive fashion with another two susceptible loci, each on chromosome 9 and 7 [23].

Analytical, diagnostic and therapeutic context of Edpm9

• By in situ hybridization with the mouse xpg probe, the rat homolog of the mouse xpg was localized on q22.3 band of rat chromosome 9, which has been known to have a conserved linkage homology to mouse chromosome 1 [24].

References