Transmembrane form of the kit ligand growth factor is determined by alternative splicing and is missing in the SId mutant

@article{Flanagan1991TransmembraneFO,
  title={Transmembrane form of the kit ligand growth factor is determined by alternative splicing and is missing in the SId
 mutant},
  author={J. Flanagan and David C. Chan and Philip Leder},
  journal={Cell},
  year={1991},
  volume={64},
  pages={1025-1035}
}
Consequences of exclusive expression in vivo of Kit-ligand lacking the major proteolytic cleavage site.
TLDR
KL-2 may substitute for KL-1 in most situations with the exception of the production of mast cells, and induced proteolytic cleavage of KL- 1 to produce soluble KL may have a role in the regeneration of hematopoietic tissue after radiation injury.
Alternative Forms and Functions of the c-kit Receptor and Its Ligand During Spermatogenesis
In both W and SI mice mutants, one major symptom, together with anemy and pigmentation defects, is sterility. In W mutants the defect is intrinsic to stem cells of the affected lineage, whereas in SI
Membrane-bound Steel factor induces more persistent tyrosine kinase activation and longer life span of c-kit gene-encoded protein than its soluble form.
TLDR
Flow cytometric analysis and pulse-chase studies showed that SI4-h248 induced rapid downmodulation of cell-surface c-kit expression and its protein degradation in MO7e cells, whereas SI 4-h220 induced more prolonged life span of c-Kit protein.
A Specific Endoplasmic Reticulum Export Signal Drives Transport of Stem Cell Factor (Kitl) to the Cell Surface*
TLDR
It is demonstrated that intracellular transport of Kitl to the cell surface is driven by a motif in the cytoplasmic tail that acts independently of the previously described basolateral sorting signal.
Transmembrane kit ligand cleavage does not require a signal in the cytoplasmic domain and occurs at a site dependent on spacing from the membrane.
TLDR
The effects of deletion or insertion variants of KL suggest that cleavage may be limited to sites within a specific range of distances from the cell membrane, which appears to differ from transforming growth factor-alpha, which apparently requires a C-terminal valine as a signal for cleavage.
Structure‐function analyses of the kit receptor for the steel factor
TLDR
It appears that Kit has at least two functions: ligand binding and ligand‐induced receptor dimerization, in addition to the kinase activity, which is independent of the transmembrane and cytoplasmic domains.
Role of p 38 and ERK MAP kinase in proliferation of erythroid progenitors in response to stimulation by soluble and membrane isoforms of stem cell factor
TLDR
The results suggest that different isoforms of SCF may use different biochemical pathways in stimulation of survival and/or proliferation of erythroid cells.
Biochemical and Genetic Characterization of Multiple Splice Variants of the Flt 3 Ligand
TLDR
The message for FL is unusually ubiquitous, whereas that of its receptor is quite restricted, apparently limiting the function of the ligand to fetal development and early hematopoiesis.
Developmental abnormalities in Steel17H mice result from a splicing defect in the steel factor cytoplasmic tail.
TLDR
The nature of the germ cell defects in male and female Sl17H mice are characterized and indicate that the cytoplasmic domain of SLF is important for its normal biological function.
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References

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Embryonic expression of a haematopoietic growth factor encoded by the SI locus and the ligand for c-kit
TLDR
It is reported that SCF is expressed during embryogenesis in cells associated with both the migratory pathways and homing sites of melanoblasts, germ cells and haematopoietic stem cells, suggesting that the receptor–ligand system has additional roles in embryogenesis.
Candidate ligand for the c‐kit transmembrane kinase receptor: KL, a fibroblast derived growth factor stimulates mast cells and erythroid progenitors.
TLDR
A mast cell proliferation assay is used to purify a 30 kd protein, designated KL, from conditioned medium of Balb/3T3 fibroblasts to apparent homogeneity and KL stimulates the proliferation of normal bone marrow derived mast cells but not mast cells from W mice, although both normal and mutant mast cells respond similarly to IL‐3.
The proto-oncogene c-kit encoding a transmembrane tyrosine kinase receptor maps to the mouse W locus
TLDR
Observations provide the first example of a germ-line mutation in a mammalian proto-oncogene and implicate the c-kit gene as a candidate for the W locus and provide a molecular entry into this important region of the mouse genome.
Expression of c-kit gene products in known cellular targets of W mutations in normal and W mutant mice--evidence for an impaired c-kit kinase in mutant mice.
TLDR
It is demonstrated that the c-kit associated tyrosine-specific protein kinase is functionally impaired in W/WV mast cells, thus providing a molecular basis for understanding the developmental defects that result from mutations at the W locus.
Developmental expression of c-kit, a proto-oncogene encoded by the W locus.
TLDR
Developmental expression of the c-kit proto-oncogene, a receptor tyrosine kinase encoded by the W locus, was investigated by in situ hybridization in normal mouse embryos and activity is complex and appears in multiple tissues including those that also display defects in mutations at the W Locus.
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