Table 2.

Genetic data

MutationType of mutationPredicted residual protein functionPhenotype
c.211G>A (p.Glu71Lys) Homozygous Missense Partial loss (hypomorphic) IBD 
c.1008C>G (p.Y336X)+c.1479delG (p.L493fsX13) Compound heterozygous Nonsense+ None (loss of function) HMIA 
frameshift 
c.975G>A (p.R325Q) Homozygous Missense Partial loss (hypomorphic) IBD 
c.313_316delTATC+c.1479delG (p.L493fsX13) Compound heterozygous Frameshift/premature stop + splice site None (loss of function) IBD 
c.2356-1G>A Homozygous Canonical splice acceptor None (loss of function) HMIA 
c.1373G>A (p.Cys458Tyr)+c.1433T>C (p.Leu478Pro) Compound heterozygous Missense + missense Partial loss (hypomorphic) IBD 
c.1433T>C (p.L478P)+c.2495C>T (p.A832V) Compound heterozygous Missense + missense Partial loss (hypomorphic) IBD 
p.Ser539Leu+p.Ala839Thr Compound heterozygous Missense + missense Partial loss (hypomorphic) IBD 
p.Gly173Val+p.Leu452Pro Compound heterozygous Missense + missense Partial loss (hypomorphic) IBD 
c.295A>G (p.M99V) Homozygous Missense Partial loss (hypomorphic) HMIA 
c.1190delCA Homozygous Frameshift None (loss of function) HMIA 
c.192delT (p.Phe64Leufs*15) Homozygous Frameshift None (loss of function) HMIA 
c.1073G>A (p.Arg358Gln) Homozygous Missense Partial loss (hypomorphic) HMIA 
c.518G>A (p.Gly173Asp)+ Compound heterozygous Missense+ Partial loss (hypomorphic)+ HMIA 
c.100_1001+2delAAGT+ Frameshift/splice+ None (loss of function)+ 
c.2170C>A (p.Gln724Lys) Missense Partial loss (hypomorphic) 
c.1001+3_1001+6del+ Compound heterozygous Splice region+ Likely loss of function HMIA 
c.2470dup+ Frameshift+ None (loss of function) 
c.1364C>A (p.Ala455Asp) Missense Partial loss (hypomorphic) 
c.517+1G>C+c.2225-2A>G Compound heterozygous Splice site (donor) + splice site (acceptor) None (loss of function) HMIA 
c.728C>A (p.Ala243Asp)+ Compound heterozygous Missense Partial loss (hypomorphic) HMIA 
c.1480T>C (p.Gly494Cys) 
c.1027G>A (p.Gly343Ser)+ Compound heterozygous Missense Partial loss (hypomorphic) IBD 
c.2405T>C (p.Ile802Thr) 
c.765_1065del (p.N256Qfs*7) Homozygous Frameshift None (loss of function) HMIA 
c.185-517del + c.185-348del Compound heterozygous Intronic deletion Partial loss (hypomorphic) HMIA 
c.1709A>G (p.His570Arg) Homozygous Missense Partial loss (hypomorphic) HMIA 
c.189C>G (p.D63E)+ Compound heterozygous Missense+ Partial loss (hypomorphic)+ HMIA 
c.412C>T (p.R138X) Nonsense None (loss of function) 
c.1636C>T (p.Arg546Trp) Homozygous Missense Partial loss (hypomorphic) HMIA 
c.1569-2A>G+ Compound heterozygous Spice site (acceptor) None (loss of function)+ HMIA 
c.1571C>T (p.A524V) Missense Partial loss (hypomorphic) 
p.Glu191fs+ Compound heterozygous Frameshift+ None (loss of function)+ HMIA 
p.Ile854Phe Missense Partial loss (hypomorphic) 
c.900C>G (p.Tyr300*)+ Compound heterozygous Nonsense+ None (loss of function)+ HMIA 
c.1213C>T (p.Arg405Cys) Missense Partial loss (hypomorphic) 
p.Glu71Lys+ Compound heterozygous Missense+ Partial loss (hypomorphic)+ HMIA 
p.Glu96 Nonsense None (loss of function) 
p.Gly45_Ala55del Homozygous In-frame deletion Partial loss of function HMIA 

List of the identified mutations in our population of patients and correlation with the presented clinical phenotype. IBD, inflammatory bowel disease; HMIA, hereditary multiple intestinal atresia.

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