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Three different cDNAs encoding mouse D-factor/LIF receptor
M Tomida1, Y Yamamoto-Yamaguchi, M Hozumi
1Department of Chemotherapy, Saitama Cancer Center Research Institute, Inc.
Journal of Biochemistry
|March 1, 1994
Summary
Researchers isolated mouse differentiation-stimulating factor (D-factor)/leukemia inhibitory factor (LIF) receptor cDNAs, identifying a soluble form. This soluble receptor, abundant in the liver, is produced via alternative mRNA processing.
Area of Science:
- Molecular Biology
- Genetics
- Biochemistry
Background:
- Differentiation-stimulating factor (D-factor), also known as leukemia inhibitory factor (LIF), plays a crucial role in cellular differentiation.
- Understanding the receptor for D-factor/LIF is essential for elucidating its biological functions.
Purpose of the Study:
- To isolate and characterize cDNAs encoding the mouse differentiation-stimulating factor (D-factor)/leukemia inhibitory factor (LIF) receptor.
- To identify potential isoforms of the D-factor/LIF receptor, including soluble forms.
Main Methods:
- Isolation of mouse liver cDNAs using a probe derived from human sequences.
- RT-PCR (Reverse Transcription Polymerase Chain Reaction) for probe preparation.
- Sequence analysis to identify receptor domains and alternative splicing events.
Main Results:
- Three cDNAs for the mouse D-factor/LIF receptor were isolated, showing high homology to the human counterpart.
- A soluble receptor isoform was identified, resulting from a 501 bp insertion that introduces a premature stop codon.
- Alternative polyadenylation of the soluble receptor mRNA leads to two distinct transcript sizes (2.6-3 kb and >5 kb), with shorter transcripts being highly abundant in the liver.
Conclusions:
- The mouse D-factor/LIF receptor exists in at least two forms: a full-length cellular receptor and a soluble receptor.
- The soluble D-factor/LIF receptor is generated through alternative splicing and exhibits differential mRNA processing, with abundant expression in the liver.
- These findings provide insights into the molecular mechanisms regulating D-factor/LIF signaling and receptor availability.