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The results of this study suggest that NAR (show CPSF4 Proteins) relieves Lop-induced constipation by increasing the levels of interstitial cells of Cajal markers (c-Kit and SCF (show KITLG Proteins)), as well as AQP3 (show AQP3 Proteins). Thus, NAR (show CPSF4 Proteins) may be effective as a candidate in patients suffering from lifestyle-induced constipation.
Among the cardiac c-kit(pos) cell cohort only a very small fraction has the phenotype and the differentiation/regenerative potential characteristics of true multipotent CSCs.
data suggest that c-Kit negatively regulates bone turnover, and disrupted c-Kit signaling couples increased bone resorption with bone formation through osteoclast-derived Wnt (show WNT2 Proteins) 10 b
Data collectively argue that mutations perturbing SCO1 function have tissue-specific consequences for the machinery that ultimately governs copper homeostasis, and further establish the importance of aberrant mitochondrial signaling to the etiology of copper handling disorders.
After intestinal myenteric plexus ablation with benzalkonium chloride, adult neurogenesis was significantly induced in c-kit loss-of-function mutant mice (W/W(v)). Imatinib induced appearance of ectopic neurons after BAC treatment, even in wildtype mice. Adult neurogenesis in the enteric nervous system is negatively regulated by c-Kit signaling in vivo.
This study indicated that c-Kit could be used as a potential therapeutic target for treatment of cardiac fibrosis.
Activation of c-kit signalling by SCF (show KITLG Proteins) promotes migration of cardiac stem cells with increased phosphorylation of CXCR4 (show CXCR4 Proteins)-serine 339, p38 mitogen-activated protein kinase (p38 MAPK (show MAPK14 Proteins)) and extracellular regulated protein kinases 1/2 (ERK1/2).
c-Kit(+) Adipose tissue-derived mesenchymal stem cells (ASCs)may promote breast cancer growth and angiogenesis by a synergistic effect of c-Kit and IL-3. Our findings suggest that c-Kit(+) subpopulations of ASCs should be eliminated in fat grafts for breast reconstruction of cancer patients following mastectomy.
exposure of HSPCs to SCF and diminished number of c-Kit receptors in their cell membranes do not compromise the capacity of HSPCs to reconstitute damaged hematopoietic tissue.
the stem cell gene Kit is regulated inversely from Krt5 (show KRT5 Proteins)/Krt14 (show KRT14 Proteins) by RA signaling
Results find that COA6 associates with COX2 and is crucial for its maturation and complex IV biogenesis. Also, COA6 interacts with the copper chaperone SCO1 which indicates that COA6 is intrinsically involved in the copper delivery process for COX2.
Sco1 is a metallochaperone that selectively transfers Cu(I) ions based on loop recognition, whereas Sco2 is a copper-dependent thiol reductase of the cysteine ligands in the oxidase.
COX20 cooperates with SCO1 and SCO2 (show SCO2 Proteins) to mature COX2 and promote the assembly of cytochrome c (show CYCS Proteins) oxidase.
COX19 (show COX19 Proteins) is necessary for the transduction of a SCO1-dependent mitochondrial redox signal that regulates ATP7A (show ATP7A Proteins)-mediated cellular copper efflux.
Results describe the tissue distribution of SCO1 and SCO2 in mouse and human tissues.
SCO1 facilitates the transfer of copper from SCO2 (show SCO2 Proteins) to the CuA site at an early stage of COX (show COX8A Proteins) assembly in mitochondria.
data suggest that both Cu(I) and Cu(II) binding are critical for normal Sco (show SNAI1 Proteins) function.
Cox17-mediated copper metallation of Sco1, as well as the subsequent failure of Cu(A) site maturation, is the basis for the inefficient assembly of the cytochrome c oxidase complex in SCO1 patients
Sco1 has evolved to bind a metal atom via the di-Cys (show DNAJC5 Proteins) motif to act as a copper chaperone, the oxidized form of the nickel-bound protein suggests that it may also maintain the thioredoxin (show TXN Proteins) function.
These results suggest a mitochondrial pathway for the regulation of cellular copper content that involves signaling through SCO1 and SCO2, perhaps by their thiol redox or metal-binding state.
Mammalian cytochrome c oxidase (COX) catalyzes the transfer of reducing equivalents from cytochrome c to molecular oxygen and pumps protons across the inner mitochondrial membrane. In yeast, 2 related COX assembly genes, SCO1 and SCO2 (synthesis of cytochrome c oxidase), enable subunits 1 and 2 to be incorporated into the holoprotein. This gene is the human homolog to the yeast SCO1 gene.
Dominant white spotting
, Steel Factor Receptor
, c-kit proto-oncogene protein
, dominant spotting
, mast/stem cell growth factor receptor Kit
, proto-oncogene c-Kit
, proto-oncogene tyrosine-protein kinase Kit
, spotted sterile male
, tyrosine-protein kinase Kit
, protein SCO1 homolog, mitochondrial
, SCO cytochrome oxidase deficient homolog 1