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1 ies difference in interpulse interval may be oligogenic.
2 gous deleterious alleles, and (3) contribute oligogenic alleles by combining point mutations and exon
3 d modeling the genetic architecture of other oligogenic and multifactorial diseases.
4 netic changes, somatic mutations, epistasis, oligogenic and polygenic hypotheses.
5              Rheumatoid arthritis (RA) is an oligogenic autoimmune disease but, to date, linkage and
6 ne disease, showed significant linkage of an oligogenic autoimmune susceptibility locus, termed AIS1,
7 e of familial and sporadic ALS, the proposed oligogenic basis for the disease, and how each new genet
8  in contrast to the previously characterized oligogenic basis of a pollinator shift in close relative
9 genic variant (P = 0.001) consistent with an oligogenic basis of amyotrophic lateral sclerosis.
10       Instead, resistance appears to have an oligogenic basis.
11 rung disease (HSCR) is a partially penetrant oligogenic birth defect that occurs when enteric nervous
12 usal genes in HCM is, in part, because of an oligogenic cause, wherein the pathogenic variants do not
13       We posit that a subset of HCM might be oligogenic caused by multiple pathogenic variants that d
14       Viewing isolated GnRH deficiency as an oligogenic condition has implications for understanding
15                                    Moreover, oligogenic cosegregation was suggestive for complex inhe
16 however, the precise genetic architecture of oligogenic diseases remains unknown.
17 ese methods for the dissection of late-onset oligogenic diseases.
18 ditory-visual synesthesia is likely to be an oligogenic disorder subject to multiple modes of inherit
19  with an interpretation of EOP as a complex, oligogenic disorder, with IL-1 genetic variation contrib
20  Bardet-Biedl syndrome (BBS), a pleiotropic, oligogenic disorder.
21                        A spectrum of complex oligogenic disorders called the ciliopathies have been c
22 ic and common polygenic diseases lie diverse oligogenic disorders involving mutations in more than on
23 ovel insights into incomplete penetrance and oligogenic effects underlying CHDs.
24 ply that human essential hypertension has an oligogenic element (a few genes may be involved in deter
25       If the genetic effects are mediated by oligogenic epistasis, as studies in the mouse suggest, i
26 se an hypothesis of a developmental phase of oligogenic expression that is followed by positive and n
27 e effects, to predict polygenic (height) and oligogenic (fusiform rust resistance) traits in a struct
28 is associated with induction of the obligate oligogenic gene Olig2.
29 nificantly (P < 0.01) lower rate, suggesting oligogenic heterozygosity as a new potential mechanism i
30             Additionally, multiple events of oligogenic heterozygosity were seen, affecting 23 of 339
31 logy revealed that controls were carriers of oligogenic heterozygous events at significantly (P < 0.0
32  families, and the disorder is thought to be oligogenic in origin.
33 that IBD comprises a heterogeneous family of oligogenic inflammatory disorders in which the specific
34 t a polygenic model with some evidence of an oligogenic influence (i.e., a handful of loci being resp
35                Elucidating the principles of oligogenic inheritance and mechanisms of genetic interac
36 uenced the age of symptom onset and supports oligogenic inheritance as relevant to disease pathogenes
37                                      Because oligogenic inheritance has been described for the relate
38                                              Oligogenic inheritance implies a role for several geneti
39                                   We studied oligogenic inheritance in Parkinson's (PD) by assessing
40 econd MKS gene, CEP290; p.R2210C, suggesting oligogenic inheritance in this disorder.
41          Together, the data suggest that the oligogenic inheritance of rare Mendelian variants may be
42                                 Here we show oligogenic inheritance of S-HSCR, the 3p21 and 19q12 loc
43         These studies are consistent with an oligogenic inheritance, in which synergistic interaction
44 ith tooth agenesis in 2 families, suggesting oligogenic inheritance.
45  genetic basis of phenotypic variability and oligogenic inheritance.
46 whole genome de novo assembly also supported oligogenic inheritance; implicating 13 genes involved in
47 plemented in the computer package Sequential Oligogenic Linkage Analysis Routines (SOLAR, San Antonio
48 inear Mixed Model) and SOLAR-MGA (Sequential Oligogenic Linkage Analysis Routines -Major Gene Analysi
49  variance component models in the Sequential Oligogenic Linkage Analysis Routines software program.
50 ve been implemented in the SOLAR (Sequential Oligogenic Linkage Analysis Routines) computer package.
51        METHODS AND We used SOLAR (Sequential Oligogenic Linkage Analysis Routines) to evaluate herita
52 onent model implemented in SOLAR (Sequential Oligogenic Linkage Analysis Routines) to evaluate linkag
53 ts methods, implemented in SOLAR (Sequential Oligogenic Linkage Analysis Routines), to estimate herit
54 s analysis, as implemented in the Sequential Oligogenic Linkage Analysis Routines, was used to estima
55 (25-75%)/FVC were performed using Sequential Oligogenic Linkage Analysis Routines.
56 ng the power to detect multiple QTLs through oligogenic linkage analysis.
57 sing Bayesian Markov chain Monte Carlo joint oligogenic linkage and association analysis, we detected
58 hy, which we speculate to be consistent with oligogenic mechanisms resulting in pleiotropic outcomes.
59 ecessive trait, recent data have unmasked an oligogenic mode of disease transmission, in which mutati
60 sively in the bilateral cases, suggesting an oligogenic mode of inheritance.
61               Our linkage results support an oligogenic model for IGE, with strong evidence for a loc
62 ting in humans, which is consistent with the oligogenic model suggested for nonsyndromic oral clefts.
63 tifactorial mode of inheritance alone, or an oligogenic model with some evidence of a recessive compo
64 t disease that fits most accurately into the oligogenic, multifactorial class of genetic diseases.
65 regating in these families, suggests complex oligogenic patterns of inheritance for ARMD.
66  be a relatively powerful design for mapping oligogenic QTL.
67 eme sibpairs (ESP) methods to detect complex oligogenic quantitative trait loci (QTL) are investigate
68  be useful for development of cultivars with oligogenic resistance that are expected to provide broad
69 se results indicate that PI 567324 possesses oligogenic resistance to the soybean aphid.
70 l as the contribution of apoE and sex, in an oligogenic segregation analysis of 75 families (742 indi
71                                 We performed oligogenic simultaneous segregation and linkage analyses
72 isk for hypertension is due to multiple (ie, oligogenic) susceptibility loci.
73 hods allow multipoint linkage analysis under oligogenic trait models in pedigrees of arbitrary size;
74 her as a simple Mendelian recessive or as an oligogenic trait, since mutations at two loci are someti
75  accuracy increase was only observed for the oligogenic trait.
76                                       We use oligogenic-trait segregation analysis to estimate the nu
77 sess the ability of predicting polygenic and oligogenic traits controlled by different levels of domi
78 Analysis Workshop; this data set had several oligogenic traits, generated by use of a 1,497-member pe
79      Potato resistance to S. endobioticum is oligogenic with one major and several minor resistance l
80                      Inheritance seems to be oligogenic, with genotype at BAAT modifying penetrance i

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