anti-KIT (KIT) 抗体产品概述

Human Mast/stem Cell Growth Factor Receptor (KIT) interaction partners

1. study was commenced to elucidate the structural behavior of this mutation in the JM and A-loop region of c-Kit using Molecular Dynamics (MD) simulations of the wild-type and mutant c-Kit in unphosphorylated and phosphorylated states

2. joint bioinformatics analysis was performed to identify the differentially expressed genes (DEGs) in wildtype Gastrointestinal stromal tumors (GISTs)samples compared with KIT/PDGFRA mutant GIST samples

3. Study of KIT mutations in Chinese children with core-binding factor-acute myeloid leukemia (CBF-AML) reveal a KIT mutation prevalence of 30% in CBF-AML and mutations are clustered in exons 17 and 8 and none in exon 10. Mutant KIT affecting exon 8 or exon 17 is correlated with shorter overall survival and event-free survival, and the influence on outcome is mutation location-dependent.

4. Findings indicated that miR-494 synergistically suppressed GISTs by concomitantly targeting survivin and KIT.

5. Mutations of the KIT gene may affect the structure and function of the transmembrane receptor KIT, which lead to Piebaldism.

6. A genetic analysis revealed a novel heterozygous mutation c.645_650delTGTGTC which results in the in-frame deletion of Val216 and Ser217 in the extracellular domain of KIT in case of familial piebaldism. Mutant KIT was able to form a heterodimer with Wt KIT and bind SCF; however, the phosphorylation of KIT, STAT5 and ERK1/2 was markedly decreased.

7. These results suggest that, in leukaemic lymphoblasts, c-Kit triggers a signalling pathway with proliferative and anti-apoptotic effects; information to this effect has not yet been reported in the literature

8. KIT and PDGFRA mutations account for 85-90% of GISTs; subsequent genetic studies have led to the identification of mutation/epimutation of additional genes, including the succinate dehydrogenase (SDH) subunit A, B, C, and D genes.

9. Data show that Kit autophosphorylation is spatio-temporally regulated and may offer a new strategy for treating imatinib-resistant gastrointestinal stromal tumours (GISTs) .

10. combined panel had the highest sensitivity and specificity at 96.3% and 100%, which was significantly or marginally higher than those of EZH2, C-KIT, and CD205 alone

11. The results show that KIT mutations and CD-117 overexpression in vulvar melanomas markers of better progression free survival.

12. current c-Kit reporter models are discussed with respect to myocardial c-Kit cell biology and function.

13. Cytoplasmic membrane CD117 immunoreactivity was demonstrated in only four (15%) out of 27 squamous cell carcinoma of the esophagus and in none of the controls.

14. a D816V-positive result in a screening blood sample identifies systemic mastocytosis among patients with hymenoptera venom-induced anaphylaxis in whom the diagnosis would most probably have been missed

15. PKC-delta expression is associated with KIT expression and the prognosis of patients with adenoid cystic carcinomas (AdCCs), suggesting that PKC-delta may be a potential therapeutic target for AdCCs.

16. Findings show that CD117 is negative in the majority of tumors with superficial features of in-situ or invasive squamous cell carcinoma and deeper, infiltrative islands with glandular differentiation, supporting that cutaneous adenosquamous carcinoma might be closer to being a variant of squamous cell carcinoma than an adnexal carcinoma.

17. Study demonstrates that an oncogenic tyrosine kinase mutant, KIT(D816V), can alter the transcriptional program of the transcription factor MITF in melanoma.

18. High c-kit expression is associated with small cell lung cancer.

19. The expression of c-Kit under the influence of nilotinib, dasatinib, erlotinib, gefitinib and afatinib was studied in HPV-positive head and neck squamous cell carcinomas. Gefitinib significantly increased cKIT expression in HPV-positive and HPV-negative head and neck squamous cell carcinoma cells whereas nilotinib and afatinib decreased cKIT expression in HPV-positive SCC.

20. CD117 can be a useful marker to help differentiate plasmablastic plasma cell myeloma from plasmablastic lymphoma

Mouse (Murine) Mast/stem Cell Growth Factor Receptor (KIT) interaction partners

1. IGF-1 upregulated c-kit expression in c-kit-positive C-kit-positive cardiac stem cells (CSCs) resulting in enhanced CSC proliferation and migration by activating the PI3K/AKT/DNMT signaling pathway to epigenetically silence miR-193a, which negatively modifies the c-kit expression level.

2. these observations imply that the expression of c-kit in the colonic epithelium is involved in the proliferation and permeability of the colonic epithelium.

3. our study demonstrated that miR-143 mediates oxidative stress-induced autophagy to enhance the survival of c-kit(+) CPCs by targeting Atg7, which will provide a complementary approach for improving cardiac progenitor cells (CPCs)-based heart repair

4. This study provides evidence that c-Kit signaling is required during arteriogenesis. Also, it strongly suggests a vascular role for c-Kit signaling because rescue of systemic c-Kit activity by bone marrow transplantation did not augment the functional recovery of Kit(W/W-v) mouse hindlimbs.

5. The results of this study suggest that NAR relieves Lop-induced constipation by increasing the levels of interstitial cells of Cajal markers (c-Kit and SCF), as well as AQP3. Thus, NAR may be effective as a candidate in patients suffering from lifestyle-induced constipation.

6. 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.

7. 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 10 b

8. Kit mutation is associated with gastrointestinal stromal tumor.

9. 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.

10. 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.

11. This study indicated that c-Kit could be used as a potential therapeutic target for treatment of cardiac fibrosis.

12. Activation of c-kit signalling by SCF promotes migration of cardiac stem cells with increased phosphorylation of CXCR4-serine 339, p38 mitogen-activated protein kinase (p38 MAPK) and extracellular regulated protein kinases 1/2 (ERK1/2).

13. 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.

14. 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.

15. the stem cell gene Kit is regulated inversely from Krt5/Krt14 by RA signaling

16. TPO and its receptor Mpl are dispensable for platelet survival in adult mice

17. Artificially applied c-kit(+) cells interact with the target organ endothelium following ischemia reperfusion injury. This interaction seems to depend on TLR-MyD88 signaling.

18. a critical role for PRL2 phosphatase in mediating Notch and c-Kit signals in early T cell progenitors, is reported.

19. These results suggest that CD44(+)CD117(+) T cells are stem cells and a specific T-cell phenotype that initially develops in the thymus, but they do not progress through DN3 and DN4 stages, lack a DP stage, and potently suppress T-cell proliferation and modulate the CTLA-4 pathway.

20. we studied the efficacy of ACK2, an antibody that blocks KIT, followed by low-dose irradiation as a preconditioning regimen for hematopoietic cell transplantation using a murine model of Mucopolysaccharidosis type II.

Cow (Bovine) Mast/stem Cell Growth Factor Receptor (KIT) interaction partners

1. it is likely that ectopic position of the KIT gene, associated with color sidedness, reflects involvement of B. taurus in the Nguni ontogeny

2. Results suggest a role of the KIT gene in determining the S(H) allele(s) in the Hereford, but not in Holstein, suggesting that complex mechanisms (or other genes) might be the cause of the spotted phenotype in this breed.

3. FGF7 may be an important regulator for oocyte growth and its action is mediated via the KIT/KITLG signaling pathway.

4. presence of KIT variants in granulosa and thecal cells of the follicle and endothelial and steroidogenic cells of the corpus luteum

Pig (Porcine) Mast/stem Cell Growth Factor Receptor (KIT) interaction partners

1. These results suggest that DDX4 and c-kit are putative markers of undifferentiated spermatogonia in the prepubertal porcine testis.

2. A simple, rapid method, with high specificity and stability, for the detection of the KIT genotype in pigs was established using TaqMan MGB probe real-time quantitative PCR.

3. mRNA expression of c-kit and SCF was decreased in gallbladder tissues in the HCD group. Consistent with the findings of RT-PCR, a lower expression level of c-kit and SCF protein was also observed in HCD animals.

4. Delayed enrichment for c-kit and inducing cardiac differentiation attenuated protective effects of BMSCs' transplantation in pig model of acute myocardial infarction.

5. It appears that the KIT gene would not be a major causal gene for melanoma development in pig, its genetic variation could be influencing this trait. Of 10 coding SNPs, three were non-synonymous mutations, likely to affect the protein conformation.

6. Study analysed KIT gene in several pig breeds and populations with different coat colours and patterns, genotyping a few polymorphisms; the 21 exons and parts of the intronic regions were sequenced in these pigs and 69 polymorphisms were identified.

7. Mutational analysis of the KIT loci in relation to coat color.

8. Variations in the KIT gene are associated with coat color.

9. The Chinese aboriginal Rongchang white pig does not carry the KIT dominant white allele present in Western white pig breeds.

10. KIT-KL might not be associated with the growth initiation of porcine primordial oocytes, although they do enhance the survival of the oocytes

11. Pravastatin improves function in hibernating myocardium by mobilizing CD133+ and cKit+ bone marrow progenitor cells and promoting myocytes to reenter the growth phase of the cardiac cell cycle.

Horse (Equine) Mast/stem Cell Growth Factor Receptor (KIT) interaction partners

1. PAX3 gene and sabino1 of KIT gene interact to create different coat color patterns

2. a splice site mutation in KIT is responsible for all white coat color phenotypes

3. a new structural deletion variant at the KIT gene; The W22 allele probably represents a null allele at the KIT gene; All horses with the W20/W22 genotype were completely white, whereas the degree of depigmentation in animals with the W22/+ genotype varied between ~15% and 100%.

4. the missense mutation p.Arg682His, the g.77784972T>C variant at KIT and the g.20147039C>T variant at MITF are the main influence on the extent of white facial markings

5. This study will provide fundamental genetic information for evaluating the genetic diversity of Kit gene in Chinese indigenous horse breeds.

6. A heterozygous splice site mutation in intron 8 of the KIT gene (c.1346 + 1G>A) in a bay Swiss Warmblood horse with extended white speckled areas.

7. Accumulating mutations in series of haplotypes at the KIT and MITF loci are major determinants of white markings in Franches-Montagnes horses.

8. The formation of the epidermal melanoblast and melanin relies on the expression of kit gene, which determines the presence of white phenotype.

9. These results indicate that the dominant white color in Franches-Montagnes Horses is caused by a nonsense mutation in the KIT gene.

10. Tobiano associated with a large paracentric chromosome inversion on horse chromosome 3, is reported, which may disrupt regulatory sequences for the KIT gene and cause the white spotting pattern.

Goat Mast/stem Cell Growth Factor Receptor (KIT) interaction partners

1. c-kit is primarily expressed in the spermatogonia and spermatocytes of goat testes.

Zebrafish Mast/stem Cell Growth Factor Receptor (KIT) interaction partners

1. The expression of c-kit and beta-catenin suggests that erythropoietin may exert a role in regeneration reducing the extent of tubular damage from the outset after gentamicin administration.

2. strong evidence for a Kit-mediated bi-directional communication system in the zebrafish ovarian follicle

3. The role of ErbB and Kit signalling in establishing melanophore stem cells in zebrafish.

4. The regeneration defect in kita mutants is not due to defects in melanocyte stem cells recruitment or in the proliferation, differentiation or survival of the daughter cells, but is instead due to a defect in stem cell establishment.

5. Kita driven expression of oncogenic HRAS leads to early onset and highly penetrant melanoma in zebrafish

6. melanocyte changes its response to Kit receptor signaling and function during development, first to promote migration, then to promote survival through distinct Kit-dependent mechanisms.

7. kit is required for melanocyte differentiation in zebrafish when melanoblast development is delayed.

8. Ectopic expression of foxd3 indicates that foxd3 promotes early melanophore death only when kit is inactive