Incontinentia pigmenti (Bloch–Sulzberger syndrome)
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Elsevier
Reference86 articles.
1. A recurrent deletion in the ubiquitously expressed NEMO (IKK-gamma) gene accounts for the vast majority of incontinentia pigmenti mutations;Aradhya;Hum Mol Genet,2001
2. Atypical forms of incontinentia pigmenti in male individuals result from mutations of a cytosine tract in exon 10 of NEMO (IKK-gamma);Aradhya;Am J Hum Genet,2001
3. Hsp70 stimulates cytokine production through a CD14-dependant pathway, demonstrating its dual role as a chaperone and cytokine;Asea;Nat Med,2000
4. Pro-inflammatory signaling: last pieces in the NF-κB puzzle?;Baeuerle;Curr Biol,1998
5. Incontinentia pigmenti: (Bloch–Sulzberger syndrome);Bambridge;Pediatrics,1953
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1. Multiple Congenital Anomalies-Hypotonia-Seizures Syndrome 2 Caused by a Novel PIGA Variant Not Associated with a Skewed X-Inactivation Pattern;Genes;2024-06-18
2. A case report of neonatal incontinentia pigmenti complicated by severe cerebrovascular lesions in one of the male monozygotic twins;Frontiers in Pediatrics;2024-05-21
3. Dysmorphic Syndromes with Skin and Skeletal Anomalies;Prenatal Diagnosis of Fetal Osteopathologies;2024
4. NEMO reshapes the α-Synuclein aggregate interface and acts as an autophagy adapter by co-condensation with p62;Nature Communications;2023-12-19
5. A case report of neonatal incontinentia pigmenti complicated by severe cerebrovascular lesions in one of the male monozygotic twins;2023-09-11
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