Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Disruption of a binding site for hepatocyte nuclear factor 4 results in hemophilia B Leyden.

15 Jul 1992

Abstract excerpt

Hemophilia B Leyden is an X chromosome-linked bleeding disorder characterized by very low plasma levels of blood coagulation factor IX (fIX) during childhood. After puberty, plasma fIX levels gradually rise to a maximum of 60% of normal, probably under the influence of testosterone. Single point mutations in the fIX promoter region of hemophilia B Leyden patients have been reported at -20, -6, -5, +8 and +13. In...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Coagulation, Bradykinin, Polyphosphates, and Angioedema
Share to Hemophilia Treatment and Research
Share to Kruppel-like factors research

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 1631121
DOI: 10.1073/pnas.89.14.6300

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Disruption of a binding site for hepatocyte nuclear factor 4 results in hemophilia B Leyden.PMID 1631121Read ↗

Hemophilia B Leyden: substitution of thymine for guanine at position - 21 results in a disruption of a hepatocyte nuclear factor 4 binding site in the factor IX promoterSemantic proximity Read ↗

Recovery from hemophilia B Leyden: an androgen-responsive element in the factor IX promoter.Semantic proximity Read ↗

Haemophilia B Leyden: the effect of mutations at position +13 on the liver-specific transcription of the factor IX gene.Semantic proximity Read ↗

Structural and functional basis of the developmental regulation of human coagulation factor IX gene: factor IX Leyden.Semantic proximity Read ↗

Disruption of a C/EBP binding site in the factor IX promoter is associated with haemophilia B.Semantic proximity Read ↗

Further evidence for the importance of an androgen response element in the factor IX promoter.Semantic proximity Read ↗

Regulatory mechanism of human factor IX gene: protein binding at the Leyden-specific region.Semantic proximity Read ↗

Synergy between transcription factors DBP and C/EBP compensates for a haemophilia B Leyden factor IX mutation.Semantic proximity Read ↗

A single base pair deletion in the promoter region of the factor IX gene is associated with haemophilia B.Semantic proximity Read ↗

Christmas disease in a Hovawart family resembling human hemophilia B Leyden is caused by a single nucleotide deletion in a highly conserved transcription factor binding site of the F9 gene promoterSemantic proximity Read ↗

Hemophilia B Leyden and once mysterious cis-regulatory mutations.Semantic proximity Read ↗

An A to T transversion at position -5 of the factor IX promoter results in hemophilia B.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.