Literature DB >> 33098248

Inherited intragenic PBX1 deletion: Expanding the phenotype.

Kristi K Fitzgerald1,2, Nina Powell-Hamilton2, Amanda J Shillingford1, Bradley Robinson1, Karen W Gripp2.   

Abstract

PBX1 encodes the pre-B cell leukemia homeobox transcription factor, a three amino acid loop extension (TALE) homeodomain transcription factor, which forms nuclear complexes with other TALE class homeodomain proteins that ultimately regulate target genes controlling organ patterning during embryogenesis. Heterozygous de novo pathogenic variants in PBX1 resulting in haploinsufficiency are associated with congenital anomalies of the kidneys and urinary tract, most commonly renal hypoplasia, as well as anomalies involving the external ear, branchial arch, heart, and genitalia, and they cause intellectual disability and developmental delay. Affected individuals described thus far have had de novo variants. Here, we report three related individuals with an inherited pathogenic intragenic PBX1 deletion with variable clinical features typical for this syndrome.
© 2020 Wiley Periodicals LLC.

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Keywords:  PBX1; congenital anomalies; intragenic deletion; variable expression

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Year:  2020        PMID: 33098248     DOI: 10.1002/ajmg.a.61932

Source DB:  PubMed          Journal:  Am J Med Genet A        ISSN: 1552-4825            Impact factor:   2.802


  1 in total

1.  Novel somatic PBX1 mosaicism likely masking syndromic CAKUT in an adult with bilateral kidney hypoplasia.

Authors:  Friederike Petzold; Wenjun Jin; Elena Hantmann; Katharina Korbach; Ria Schönauer; Jan Halbritter
Journal:  Clin Kidney J       Date:  2022-04-06
  1 in total

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