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

A mutation in Sec15l1 causes anemia in hemoglobin deficit (hbd) mice.

Nature genetics - 1 Nov 2005

Lim Jackie E, Jin Ou, Bennett Carolyn, Morgan Kelly, Wang Fudi, Trenor Cameron C, Fleming Mark D, Andrews Nancy C

Abstract excerpt

Hemoglobin deficit (hbd) mice carry a spontaneous mutation that impairs erythroid iron assimilation but does not cause other defects. Normal delivery of iron to developing erythroid precursors is highly dependent on the transferrin cycle. Through genetic mapping and complementation experiments, we show that the hbd mutation is an in-frame deletion of a conserved exon of the mouse gene Sec15l1, encoding one of two...

Read the complete abstract on PubMed

Topics

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

Share to Anemia
Share to Bone Marrow Transplantation
Share to Endosomes

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

Share to Hemoglobins

Share to rab GTP-Binding Proteins

Share to Receptors, Transferrin

Share to Retroviridae

Share to Transferrin

Source

Identifiers

PMID: 16227995
DOI: 10.1038/ng1659

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.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A mutation in Sec15l1 causes anemia in hemoglobin deficit (hbd) mice.PMID 16227995Read ↗

Loss of rapid transferrin receptor recycling due to a mutation in Sec15l1 in hbd mice.Semantic proximity Read ↗

Mutations affecting the secretory COPII coat component SEC23B cause congenital dyserythropoietic anemia type II.Semantic proximity Read ↗

New Cases and Mutations in SEC23B Gene Causing Congenital Dyserythropoietic Anemia Type II.Semantic proximity Read ↗

The mitochondrial ATP-binding cassette transporter Abcb7 is essential in mice and participates in cytosolic iron–sulfur cluster biogenesisSemantic proximity Read ↗

Characteristic phenotypes associated with congenital dyserythropoietic anemia (type II) manifest at different stages of erythropoiesis.Semantic proximity Read ↗

Abcb7, the gene responsible for X-linked sideroblastic anemia with ataxia, is essential for hematopoiesis.Semantic proximity Read ↗

A common SEC23B missense mutation in congenital dyserythropoietic anemia type II leads to growth restriction and symptoms of chronic pancreatitis in miceSemantic proximity Read ↗

Congenital dyserythropoietic anemia type II: molecular analysis and expression of the SEC23B gene.Semantic proximity Read ↗

Pancreatic SEC23B deficiency is sufficient to explain the perinatal lethality of germline SEC23B deficiency in mice.Semantic proximity Read ↗

SEC23B Loss-of-Function Suppresses Hepcidin Expression by Impairing Glycosylation Pathway in Human Hepatic Cells.Semantic proximity Read ↗

The beta subunit of the Sec61p endoplasmic reticulum translocon interacts with the exocyst complex in Saccharomyces cerevisiae.Semantic proximity Read ↗

SEC23B is required for the maintenance of murine professional secretory tissues.Semantic proximity Read ↗

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