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Xpb

Not assigned

Significant (p = 2.7 x 10-4; MLS > 3.6)

1qc

Not assigned

Suggestive (MLS = 3.31)

Note: The IDDM nomenclature is assigned to a locus after linkage has been formally demonstrated, replicated, and confirmed in at least three different datasets. Where functional candidate genes are flanked by or very close to susceptibility markers, they are indicated.

a The evidence for linkage increased substantially (p = 0.00004) with the higher density of markers and the inclusion of data for additional affected relatives and all unaffected siblings (46); NPL, nonparametric linkage.

b In major histocompatibility complex (MHC) human leukocyte antigen (HLA)-DR3 positive patients (47). c This locus (48) colocalizes with loci for systemic lupus erythematosus (SLE) (49) and ankylosing spondylitis (50).

d MLS, maximum logarithm of odds score.

Note: The IDDM nomenclature is assigned to a locus after linkage has been formally demonstrated, replicated, and confirmed in at least three different datasets. Where functional candidate genes are flanked by or very close to susceptibility markers, they are indicated.

a The evidence for linkage increased substantially (p = 0.00004) with the higher density of markers and the inclusion of data for additional affected relatives and all unaffected siblings (46); NPL, nonparametric linkage.

b In major histocompatibility complex (MHC) human leukocyte antigen (HLA)-DR3 positive patients (47). c This locus (48) colocalizes with loci for systemic lupus erythematosus (SLE) (49) and ankylosing spondylitis (50).

d MLS, maximum logarithm of odds score.

insulin gene region on chromosome 11p15 (IDDM2). The contribution of these two loci to familial inheritance is approx 42% for IDDM1 and 10% for IDDM2. As a result of genomewide searches, many other putative loci have been proposed to be related with T1DM. These loci, along with some potential candidate genes, are listed in Table 2. The fact that, in humans, the highest risk-conferring locus linked to the disease is the HLA cluster, and, in particular, HLA genes encoding specific class II alleles, strongly indicates an important role of the immune cells in both the development and the activation of the autoimmune response leading to disease onset (51,52). Interestingly, the same HLA locus seems to have the same susceptibility influence in a mouse model of T1DM, the nonobese diabetic (NOD) mouse (53) (see Table 3). The immune-mediated processes of P-cell destruction are mainly T-cell dependent and chronic in the NOD mouse (54), the Bio-Breeding (BB) rat (55), and, more than likely, in humans (51) (see Table 3). Comparative mapping of human and NOD mouse insulin-dependent diabetes (Idd) genes and phenotype/functions controlled by Idd loci are shown in Tables 3 and 4.

Table 3

Comparative Mapping of Human (IDDM) and Murine (Idd) Genes

Table 3

Comparative Mapping of Human (IDDM) and Murine (Idd) Genes

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Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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