To date, mutations in NBAS and IARS have been identified as previously unknown genetic causes of infantile hepatopathy leading to ALF [1 3].
The renal cortex (CO), the outer stripe of the outer medulla (OS), the inner stripe of the outer medulla (IS) and the inner medulla (IM) were identified as previously described [10].
Intracellular cytokines were identified as previously reported [32].
RAG-1 deficiency was identified as previously described [1], [14], [17].
Voltage-gated K+, Ca2+ and Ca2+-activated K+ (KCa) channels were identified, as previously described.
In Scopus, cited references are uniquely identified as previously published papers.
Patients and controls were identified as previously described and reported [16], [25].
Genomic regions demonstrating ultra-high conservation across species were identified as previously described [25].
Genetic interactions from SGA screens were processed and identified as previously described [26].
Uteri were dissected out and fixed in Neutral Buffered Formalin before PEGLA immunoreactivity in the vagina and uterus was identified as previously described [34].
Notably, transgenic mice developed liver cancer around 7 8 months and a tumour stage-dependent network of EGF-regulated genes was identified, as previously reported [1].
