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  • Gene
  • This gene encodes a member of an adapter protein family that binds to several tyrosine-phosphorylated proteins. (nih.gov)
  • The product of this gene has several SH2 and SH3 domains (src-homology domains) and is involved in several signaling pathways, recruiting cytoplasmic proteins in the vicinity of tyrosine kinase through SH2-phosphotyrosine interaction. (nih.gov)
  • Mutations in the ABL gene are associated with chronic myelogenous leukemia (CML), where it is activated by being translocated within the BCR (breakpoint cluster region) gene on chromosome 22. (femtopath.com)
  • ABL exon 6 primer set have the function to enrich mutation type of ABL gene and allows to detect target codons T315 on DNA samples. (femtopath.com)
  • Activation of the ABL tyrosine kinase is a primary event in the genesis of CML, as shown by the retrovirally mediated insertion of a human BCR-ABL gene into murine hematopoietic stem cells and the creation of BCR-ABL transgenic mice ( 3 ). (aacrjournals.org)
  • Washington DC, USA ---------------------------------------------------------------------------- Description: Human chromosome 9: entries, gene names and cross-references to MIM Name: humchr09.txt Release: 2018_01 of 31-Jan-2018 ---------------------------------------------------------------------------- This documents lists all the human protein sequence entries whose genes are known to be encoded on chromosome 9 in this release of UniProtKB/Swiss-Prot. (uniprot.org)
  • Several types of somatic mutations have been identified, including base substitutions, insertions, deletions, translocations, and chromosomal gains and losses, all of which result in altered activity of an oncogene or tumor-suppressor gene. (hhmi.org)
  • In one mechanism, promoter/enhancer elements of one gene are rearranged adjacent to a proto-oncogene, thus causing altered expression of an oncogenic protein. (hhmi.org)
  • The prototypic example of this translocation is the BCR-ABL gene fusion in chronic myelogenous leukemia (CML). (hhmi.org)
  • Earlier, using a bioinformatics approach to select oncogenes from a collection of microarray data ( www.oncomine.org ), we serendipitously identified a recurrent fusion of the androgen-regulated gene TMPRSS2 to the ETS family of transcription factors in the majority of prostate cancers (over 50 percent). (hhmi.org)
  • Jun proteins modulate the ovary-specific promoter of aromatase gene in ovarian granulosa cells via a cAMP-responsive element. (biomedsearch.com)
  • Ectopic expression of the Jun proteins in a human granulosa cell line significantly inhibited an ovary-specific promoter (PII) of the aromatase gene, whereas expression of dominant-negative mutants of Jun led to increased promoter activity. (biomedsearch.com)
  • Taken together, our work suggests that Jun proteins may attenuate estrogen biosynthesis by directly downregulating transcription of the aromatase gene in ovarian granulosa cells. (biomedsearch.com)
  • kinases
  • Aggressive breast cancer cells are dependent on activated Abl kinases for proliferation, anchorage-independent growth and survival. (nih.gov)
  • however little is known regarding whether Abl kinases contribute to the development or progression of solid tumors. (nih.gov)
  • We recently demonstrated that endogenous Abl kinases (c-Abl, Arg) are activated by deregulated ErbB receptors and Src kinases, and drive invasion of aggressive breast cancer cells. (nih.gov)
  • In this study, we examined whether activation of endogenous Abl kinases affects transformation, proliferation and survival, which are major contributors to breast cancer development and metastatic progression. (nih.gov)
  • Using a pharmacological inhibitor and RNAi, we demonstrate that activation of endogenous Abl kinases dramatically promotes breast cancer cell proliferation and anchorage-independent growth in serum, as well as survival following nutrient deprivation. (nih.gov)
  • Moreover, we identify IGF-1R as a novel upstream activator of endogenous Abl kinases, and demonstrate that Abl kinase activation is required for IGF-1-stimulated cell cycle progression in breast cancer cells. (nih.gov)
  • Direct DNA damage by ionizing radiation or UV can activates the interconnected apoptotic pathways by stimulation of protein kinases from phosphoinositide-3-kinases family. (bio-rad.com)
  • These stimulated kinases directly or indirectly activate phosphorylation of proteins from apoptotic pathways: tumor suppressor p53 , breast and ovarian cancer susceptibility protein 1 ( Brca1 ), E2F transcription factor 1 ( E2F1 ), proto-oncogene tyrosine-protein kinase c-Abl and cell cycle regulator RAD9 . (bio-rad.com)
  • The effect of dasatinib, an inhibitor of Src and Abl kinases, on paclitaxel sensitivity was measured in ovarian cancer cells and HEY xenografts. (ox.ac.uk)
  • RESULTS: Src family and Abl kinases were identified as modulators of paclitaxel sensitivity in SKOv3 cells. (ox.ac.uk)
  • CONCLUSION: Inhibition of Src family and Abl kinases with either siRNAs or dasatinib enhances paclitaxel sensitivity of ovarian cancer cells through p27(Kip1)-mediated suppression of Bcl-2 and Cdk1 expression. (ox.ac.uk)
  • Oncogenic forms of src-family kinases can occur through altered regulation or expression of the endogenous protein and by virally encoded src (v-src) genes. (sickkids.ca)
  • genes
  • Genes that are involved in cancer are divided into two categories: oncogene and tumor suppressor. (hindawi.com)
  • Protooncogenes are protein-coding genes that promote cell division, including growth factors (e.g., platelet-derived growth factor, epidermal growth factor, and fibroblast growth factor), growth factor receptors (e.g. (hindawi.com)
  • Tumor suppressor genes are protein-coding genes that suppress cell division, such as RB1 and p53. (hindawi.com)
  • The mission of my lab is to facilitate the discovery, validation, and implementation of candidate target genes/proteins in disease diagnosis, prognosis, and therapy. (hhmi.org)
  • This type of translocation is exemplified by the apposition of immunoglobulin and T cell receptor (TCR) genes to MYC , leading to activation of this oncogene in B and T cell malignancies, respectively. (hhmi.org)
  • In the second mechanism, the rearrangement results in the fusion of two genes, which produces a fusion protein that may have a new function or altered activity. (hhmi.org)
  • Recombinant
  • Abgent has over fifteen years of experience producing recombinant proteins in E. coli and mammalian cells (CHO and HEK293, etc), and we have added a powerful yeast expression platform to our menu of services. (abgent.com)
  • tumor
  • A reduced miR-126 expression and an elevated Crk protein expression, alone or in combination, statistically correlated with aggressive clinicopathological characteristics, such as larger tumor size, deeper local invasion, more lymph node metastasis, advanced TNM stage, and poorer prognosis. (nih.gov)
  • GRB2
  • The BCR-ABL/GRB2 complex recruits Son of Sevenless (SOS), which is constitutively associated with the GRB2 SH3 domain ( 10 ). (aacrjournals.org)
  • As a consequence, the GRB2/GAB2/SOS complex causes constitutive activation of the RAS downstream pathway, thereby activating mitogen-activated protein (MAP) extracellular signal-regulated kinase (ERK)1/2 (MEK) and MAP kinase proteins and resulting in abnormal cell proliferation. (aacrjournals.org)
  • Mice
  • When wild-type mice were treated with the hyperoxia regimen, a fivefold decrease in VEGF mRNA expression was observed from P7 to P16.However, retinal VEGF expression in hyperoxia-treated homozygous mice did not decrease and remained at control levels.These data suggest that c-abl is required for the hyperoxia-induced retinal neovascularization and hyperoxia-induced decrease in VEGF mRNA levels. (nih.gov)
  • The requirement for the nonreceptor tyrosine kinase c-abl in the pathogenesis of retinopathy of prematurity (ROP) was examined using the mouse model for ROP and c-abl-deficient mice. (nih.gov)
  • Hyperoxia-induced retinal neovascularization was observed in wild-type and heterozygous mice but animals that were homozygous for c-abl did not develop a vasoproliferative retinopathy in response to hyperoxia. (nih.gov)
  • Because VEGF is involved in the development of hyperoxia-induced retinal vasoproliferation 5 and mice deficient in c-abl failed to develop hyperoxia-induced retinopathy, we sought to determine if mice that lack c-abl could respond normally to VEGF. (nih.gov)
  • To examine if homozygous c-abl mice generate an angiogenic response to exogenously supplied VEGF, a corneal angiogenesis assay was employed 35. (nih.gov)
  • New blood vessels emerged from the limbal vasculature of wt and c-abl−/− mice toward the VEGF-saturated pellet, whereas no vessels were observed in animals with sham pellets (Fig. 5). (nih.gov)
  • These observations demonstrate that c-abl activity is not required for VEGF-induced signal transduction and that the c-abl−/− mice responded normally to the ectopic administration of VEGF. (nih.gov)
  • pathway
  • In particular, the phosphoinositide 3-kinase (PI3K)/AKT pathway can be effectively blocked by mTOR inhibitors, and several compounds can hit the RAS pathway and the resulting mitogen-activated protein (MAP) extracellular signal-regulated kinase (ERK)1/2 (MEK) and MAP kinase activation. (aacrjournals.org)
  • Mdm2
  • The ubiquitin-protein ligase E3 Mdm2 protein ubiquitinates and promotes degradation of p53 . (bio-rad.com)
  • 11 ] c-Abl neutralizes the inhibitory effect of Mdm2 on p53 . (bio-rad.com)
  • Furthermore, we demonstrate that Mdm2-mediated modification of AR and HDAC1 catalyses protein destabilization and attenuates AR sactivity, suggesting that ubiquitylation of the AR and HDAC1 may constitute an additional mechanism for regulating AR function. (ox.ac.uk)
  • Retinal Neovascularization
  • These data suggest that c-abl is required for the hyperoxia-induced retinal neovascularization and hyperoxia-induced decrease in VEGF mRNA levels. (nih.gov)
  • regulator
  • The N-terminal SH2 domain of this protein functions as a positive regulator of transformation whereas the C-terminal SH3 domain functions as a negative regulator of transformation. (nih.gov)
  • transcript
  • In this report, we show that the protein levels of gadd45α, whose transcript levels are increased during DNA damage and stress signals, are upregulated following curcumin treatment in a dose- and time-dependent manner. (nih.gov)
  • Brca1
  • Background: BAP1 (BRCA1-Associated Protein 1) was originally identified as a BRCA1 associated, nuclear localized ubiquitin hydrolase that suppresses cell growth (1). (cellsignal.com)
  • The protein belongs to the UCH family of deubiquitinases, with a UCH domain in its N-terminal segment and a BRCA1 interaction domain as well as a nuclear localization signal in its C-terminal segment (1). (cellsignal.com)
  • regulation
  • Reciprocal regulation of Abl kinase by Crk Y251 and Abi1 controls invasive phenotypes in glioblastoma. (nih.gov)
  • To investigate the biology and regulation of telomerase in CML, we evaluated expression of the telomerase components, its regulators and several telomeric-associated proteins. (ox.ac.uk)
  • Regulation of the AR is achieved by alternate binding of either histone acetyltransferase (HAT)-containing co-activator proteins, or histone deacetylase 1 (HDAC1). (ox.ac.uk)
  • expression
  • Expression of hTR and telomeric-associated proteins TEP1, TRF1, TRF2, tankyrase and PinX1 was high in the majority of CP and AP patients. (ox.ac.uk)
  • With state-of-the art molecular biology and protein biochemistry labs, we work with our clients to rapidly evaluate in parallel to identify the optimal expression system for candidate proteins. (abgent.com)
  • In the current study, we unraveled an important role of Jun proteins in modulating ovary-specific aromatase expression. (biomedsearch.com)
  • antibodies
  • Check out links to articles that cite our custom service antibodies, peptides, and proteins in major peer-reviewed journals, organized by research category. (abgent.com)
  • prognosis
  • Title: Dysregulation of miR-126/Crk protein axis predicts poor prognosis in gastric cancer patients. (nih.gov)
  • Moreover
  • 6 ] Moreover, JNK stimulates activity of proapoptotic proteins, Bcl-2 modifying factor ( BMF ) and BCL2-like 11 factor ( Bim ). (bio-rad.com)