Disease relevance of Kitl

• Stem cell factor contributes to intestinal mucosal mast cell hyperplasia in rats infected with Nippostrongylus brasiliensis or Trichinella spiralis, but anti-stem cell factor treatment decreases parasite egg production during N brasiliensis infection [1].
• Previous studies have shown that traumatic brain injury is associated with a profound decline in intracellular free magnesium (Mgf) and in total tissue magnesium (Mgt), the extent of Mgf decline being linearly correlated to the severity of injury and resultant neurological deficit [2].
• A construct in which the proximal MGF binding site in the beta-casein promoter region has been inactivated by mutation and a construct regulated by the adenovirus major late promoter served as controls [3].
• Pertussis toxin (PT) inhibited SCF-induced potentiation of IgE-dependent histamine secretion, indicating that PT-sensitive G-proteins are involved in the immediate effects of SCF [4].

High impact information on Kitl

• Partial cDNA and genomic clones of rat stem cell factor (SCF) have been isolated [5].
• Finally, using an oligonucleotide encompassing both the YY1 and MGF sites, we detected a slow-mobility complex only in extracts from mammary glands at late pregnancy and lactation (lactation-associated complex [LAC]) [6].
• Second, it was demonstrated that extracts prepared from several cell types contained a protein(s) interacting with the mammary gland-specific factor (MGF) binding site, previously shown to be required for beta-casein promoter activity (Schmitt-Ney et al., Mol. Cell. Biol. 11:3745-3755, 1991) [6].
• Ethylnitrosourea-induced rat mammary tumor cell lines were transfected with vector containing either control (no insert, C-P), sense (S-P), or antisense (AS-P) SCF DNA [7].
• The present results indicate that the signal transduction of the SCF/KIT system plays a crucial role in the development of oval cells, at least, in the rat AAF/PH model, and suggest that KIT-mediated signal transduction plays only a small role in determining the phenotype and in the proliferative activity of oval cells [8].

Biological context of Kitl

• This response was selective and associated, in ethylene dimethane sulfonate-treated animals, with a decrease in the mRNA levels of stem cell factor (SCF), i.e. a key signal in spermatogenesis and a putative regulator of Leydig cell development [9].
• Thus, the effects of ghrelin on SCF gene expression were evaluated [9].
• Also, MGF is expressed with an early upregulation in loaded tendon tissue [10].
• We investigated the inhibitory activity of nerve growth factor (NGF) on apoptosis of rat peritoneal mast cells (PMCs) and compared it with that of recombinant stem cell factor (rSCF), which is a mast cell growth factor [11].
• A subsequent proliferative response to stem cell factor (SCF), the ligand for the proto-oncogene receptor tyrosine kinase c-kit, is characterized by an initial maturation in immunophenotype and subsequent self-renewal of cells (SCF blasts) without differentiation for at least 50 generations [12].

Anatomical context of Kitl

• Stem cell factor (SCF) isolated from culture medium conditioned by Buffalo rat liver cells was subjected to detailed structural analysis [13].
• In addition, we present novel evidence for the ability of ghrelin to modulate the expression of the SCF gene, which may have implications for the mode of action of this molecule in the testis as well as in other physiological systems [9].
• However, it is not known whether MGF is expressed and upregulated in mechanically loaded tendon [10].
• Stem cell factor protects germ cells from apoptosis in vitro [14].
• Surprisingly, not only spermatogonia, but also spermatocytes and spermatids, were protected from apoptosis in the presence of SCF [14].

Associations of Kitl with chemical compounds

• The effects of rat stem-cell factor (SCF) and interleukin-3 (IL-3), alone or in combination, on the in vitro growth and serine proteinase expression of rat serosal/connective-tissue mast cells (CTMC) or bone marrow-derived mast cells (BMMC) were examined [15].
• Oval cells that develop in the rat 2-acetylaminofluorene/partial hepatectomy (AAF/PH) model express the c-kit receptor tyrosine kinase (KIT) and its ligand, stem cell factor (SCF) [8].
• SCF induced serotonin release from rat peritoneal mast cells, connective tissue-type mast cells [16].
• The treatment of rat peritoneal mast cells with SCF failed to produce inositol 1,4,5-trisphosphate, indicating the absence of involvement of phosphoinositide-specific phospholipase C pathway [16].
• PP1 inhibited SCF-induced c-Kit autophosphorylation in intact cells and blocked the activation of mitogen-activated protein kinase and Akt [17].

Regulatory relationships of Kitl

• MGF was expressed and upregulated in loaded tendon tissue with a faster response than IGF-I, which was increased from day 8 [10].
• COX-2 induction and the attendant delayed PGD2 generation in CTMC were modestly induced by c-kit ligand, but not by Fc epsilonRI cross-linking [18].
• Stem cell factor-induced signal transduction in rat mast cells. Activation of phospholipase D but not phosphoinositide-specific phospholipase C in c-kit receptor stimulation [16].

Other interactions of Kitl

• Kit ligand and basic fibroblast growth factor interactions in the induction of ovarian primordial to primary follicle transition [19].
• A splice variant of IGF-I, mechano-growth factor (MGF) is upregulated and known to be important for adaptation in loaded muscle [10].
• C-kit ligand (Stem Cell Factor) affects neuronal activity, stimulates pituitary-adrenal axis and prolactin secretion in rats [20].

Analytical, diagnostic and therapeutic context of Kitl

• Sequence analysis of this site revealed similarity to the gamma interferon-activated sequence, suggesting that MGF may be related to the stat91 signaling protein [6].
• There was a good correlation between the binding of 3H-SCF and its biological activity, as evidenced by a selective suppression of basal FSH release in pituitary cell cultures [21].
• The present study further characterized the binding of [3H]SCF to rat anterior pituitary in vitro and explored its potential use as a radioreceptor assay for SCF and other inhibin preparations [22].
• Tritium-labeled SCF (3H-SCF), synthesized by rat Sertoli cells in vitro in the presence of 3H-leucine and partly purified by Sephadex gel chromatography, was used to the ligand [21].
• Immunocytochemical analysis demonstrated the presence of stem cell factor (SCF) in proliferating oval cells during 6 weeks of copper depletion, and Northern blot analysis revealed the expression of liver-enriched transcription factors in the rat pancreas during this 4-6-week period of copper deficiency [23].

References