Activity
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9 actions
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| Primary immunodeficiency or monogenic inflammatory bowel disease v9.70 | IKBKE | Achchuthan Shanmugasundram Classified gene: IKBKE as Amber List (moderate evidence) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v9.70 | IKBKE | Achchuthan Shanmugasundram Added comment: Comment on list classification: There are two unrelated cases identified with monoallelic IKBKE variants and functional evidence is also available for these variants. However, different phenotypes were reported in these two patients (HSV-2 meningitis vs autoinflammatory disease). Hence, this gene can only be rated amber with the current evidence. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v9.70 | IKBKE | Achchuthan Shanmugasundram Gene: ikbke has been classified as Amber List (Moderate Evidence). | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v9.69 | IKBKE | Achchuthan Shanmugasundram Phenotypes for gene: IKBKE were changed from Herpes Simplex Virus type 2 (HSV-2) meningitis; Mollaret meningitis to Herpes Simplex Virus type 2 (HSV-2) meningitis; autoinflammatory syndrome, MONDO:0019751 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v9.68 | IKBKE | Achchuthan Shanmugasundram Publications for gene: IKBKE were set to 37937644 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v9.67 | IKBKE | Achchuthan Shanmugasundram Mode of inheritance for gene: IKBKE was changed from MONOALLELIC, autosomal or pseudoautosomal, imprinted status unknown to MONOALLELIC, autosomal or pseudoautosomal, NOT imprinted | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v9.66 | IKBKE | Achchuthan Shanmugasundram edited their review of gene: IKBKE: Changed phenotypes to: Herpes Simplex Virus type 2 (HSV-2) meningitis, autoinflammatory syndrome, MONDO:0019751 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v9.66 | IKBKE | Achchuthan Shanmugasundram reviewed gene: IKBKE: Rating: AMBER; Mode of pathogenicity: None; Publications: 37937644, 39524436; Phenotypes: ; Mode of inheritance: MONOALLELIC, autosomal or pseudoautosomal, NOT imprinted | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v9.9 | IKBKE |
Boaz Palterer gene: IKBKE was added gene: IKBKE was added to Primary immunodeficiency or monogenic inflammatory bowel disease. Sources: Literature Mode of inheritance for gene: IKBKE was set to MONOALLELIC, autosomal or pseudoautosomal, imprinted status unknown Publications for gene: IKBKE were set to 37937644 Phenotypes for gene: IKBKE were set to Herpes Simplex Virus type 2 (HSV-2) meningitis; Mollaret meningitis Penetrance for gene: IKBKE were set to unknown Review for gene: IKBKE was set to RED Added comment: IKBKE encodes IKKε (Inhibitor of nuclear factor kappa-B kinase subunit epsilon), a noncanonical IκB kinase that plays a nonredundant role in mediating the innate immune response to viral infections. Reyahi et al. identified a monoallelic truncating variant in IKBKE (c.312delC) as the cause of highly disabling, recurrent Herpes Simplex Virus type 2 (HSV-2) meningitis. Functional analyses demonstrate that this mutated allele encodes a truncated protein lacking kinase activity, which exerts a dominant-negative effect over the wild-type protein. This results in a functional deficiency within the cGAS/STING pathway, impaired STING phosphorylation, and a failure of patient cells (including stem cell-derived microglia) to mount an adequate IFN-β antiviral response against HSV-2 and double-stranded DNA. Sources: Literature |
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