• Note that by convention gene names are italicized and the proteins they make are not. (cancerquest.org)
  • As an example TP 53 refers to the gene and p53 refers to the protein. (cancerquest.org)
  • The translocation occurs in a primitive hematopoietic stem cell and the gene encodes a fusion protein (Bcr-Abl) that has deregulated tyrosine kinase (TK) activity and activates intracellular pathways that lead to increased cellular proliferation, resistance to apoptosis and genetic instability [1,3]. (rockstarsagainstliveearth.com)
  • Chronic myelogenous leukaemia (CML) is characterised at the molecular level by a (9;22) translocation which places the abl proto-oncogene under the control of the breakpoint cluster region (bcr) gene promoter generating a fusion protein (p210) with enhanced tyrosine kinase activity. (tcd.ie)
  • In chronic myelogenous leukemia (CML) patients, an aberrant translocation results in the replacement of the first exon of Abl with the BCR (breakpoint cluster region) gene. (umbc.edu)
  • Abl2, also known as ARG (Abelson-related gene), is thought to play a cooperative role with Abl in the proper development of the nervous system. (umbc.edu)
  • The TEL gene is a frequent fusion partner of other tyr kinase oncogenes, including Tel/Abl, Tel/PDGFRbeta, and Tel/Jak2, found in patients with leukemia and myeloproliferative disorders. (umbc.edu)
  • Within this research, we sought to determine novel splice variants with the BCLL gene, a member within the apoptosis associated BCL family members, determined by examination of EST sequences. (mirnamimic.com)
  • RB1 encodes the protein pRB and was the first tumor suppressor gene to be molecularly defined. (medscape.com)
  • This gene is a member of the protein-tyrosine kinase oncogene family. (cancerindex.org)
  • What does this gene/protein do? (cancerindex.org)
  • What pathways are this gene/protein implicaed in? (cancerindex.org)
  • Our studies have demonstrated that several of the proteins encoded by cellular oncogenes function in fundamental aspects of gene regulation. (stanford.edu)
  • 1 Mixed lineage leukemia (MLL) gene fusions are the molecular hallmark of infant acute lymphoblastic leukemia (ALL) and are present in tumor cells in up to 80% of patients. (ashpublications.org)
  • 2 Detection of the gene fusion in neonatal blood spots indicates that MLL-rearranged infant ALL originates in utero. (ashpublications.org)
  • [ 1 ] His prediction was subsequently supported by the cloning of the retinoblastoma tumor suppressor gene ( RB1 ) and by functional studies of the retinoblastoma protein, Rb. (medscape.com)
  • For example, the TP53 gene, located on chromosome 17, encodes a 53-kd nuclear protein that functions as a cell cycle checkpoint. (medscape.com)
  • The TP53 gene is also capable of stimulating apoptosis of cells containing damaged DNA. (medscape.com)
  • The determining hallmark of persistent myeloid leukemia (CML) may be the fusion gene while it began with a hematopoietic stem cell (1C4). (angiogenesis-blog.com)
  • The BCR-ABL oncoprotein (p210BCR-ABL) encoded by this gene shows constitutively raised tyrosine kinase (TK) activity that drives the pathogenesis of the condition by perturbing multiple signaling pathways, like the RAS/MAPK, PI3K/AKT, and Janus kinase 2 (JAK2)/ sign transducer and activator of transcription 5 (STAT5) pathways (5,6). (angiogenesis-blog.com)
  • The proto-oncogene tyrosine-protein kinase (BCR-ABL1) oncogenic breakpoint cluster region-protein with enhanced tyrosine kinase action is encoded by this fusion gene. (inter-publishing.com)
  • PP2A, a serine/threonine phosphatase composed of 3 distinct subunits-65-kDa PP2A-A (scaffold subunit), 55-kDa PP2A-B (regulatory subunit), and 37-kDa PP2A-C (catalytic subunit)-constitutes 0.2%-1.0% of the total protein content in mammalian cells and has been implicated in the regulation of diverse cellular processes, including signal transduction, cell cycle progression, DNA replication, gene transcription, and protein translation 5 - 8 . (cancerbiomed.org)
  • An abnormal chromosomal translocation known as t(9;22) results in the establishment of the Philadelphia chromosome, which contains the BCR-ABL gene, culminating in the development of this syndrome ( 1 ). (spandidos-publications.com)
  • The effect may be knock out an entire signalling or DNA repair pathway, the downstream effect being inappropriate promotion of the cell cycle, inappropriate gene expression, inability to trigger apoptosis, or accumulation of DNA damage. (me.uk)
  • [4] Fusion genes may be problematic because they can combine the active regions of one gene with the promoters or regulatory sites of another, or because the resultant product looses some of its functionality. (me.uk)
  • The protein encoded by this gene belongs to the pyridine nucleotide-disulfide oxidoreductase family, and is a member of the thioredoxin (Trx) system. (cancerindex.org)
  • the Philadelphia chromosome is present in 90+% of patients with high white cell counts (up to 100 to 300), and in those where it isn't present, the BCR-ABL fusion gene is generally identifiable. (mpninfo.org)
  • 05. Between the 69 ejaculated proteins, 68 may very well be linked to Gene Ontology data. (smadpathway.com)
  • During this translocation, a piece of chromosome 9 containing the oncogene ABL is translocated to chromosome 22 and fused to the BCR gene. (msdmanuals.com)
  • The chimeric fusion gene BCR-ABL is responsible for production of the oncoprotein bcr-abl tyrosine kinase. (msdmanuals.com)
  • This translocation, written as t(9;22), fuses part of the ABL1 gene from chromosome 9 with part of the BCR gene from chromosome 22, creating an abnormal fusion gene called BCR-ABL1 . (medlineplus.gov)
  • The function of the protein produced from the normal BCR gene is not completely understood, although it has been shown to help control signaling in cells. (medlineplus.gov)
  • The protein produced from the normal ABL1 gene is involved in many cellular processes, including cell growth and division (proliferation), maturation (differentiation), movement (migration), and self-destruction (apoptosis). (medlineplus.gov)
  • Like the ABL1 protein, the abnormal protein produced from the fusion gene, called BCR-ABL1, can promote cell proliferation and block apoptosis. (medlineplus.gov)
  • In 5 to 10 percent of cases of chronic myeloid leukemia, the BCR-ABL1 fusion gene is created by complex rearrangements that involve other chromosomes in addition to chromosomes 9 and 22. (medlineplus.gov)
  • In the cytoplasm, Abl plays a role in cell proliferation and survival. (umbc.edu)
  • Genetic drivers are mutations or fusions that confer a survival advantage to "drive" malignant proliferation. (medscape.com)
  • Tumor suppressor genes encode proteins that normally provide negative control of cell proliferation. (medscape.com)
  • PTEN encodes a protein kinase of the same name and functions as a tumor suppressor through regulation of cell proliferation. (medscape.com)
  • Lyn, a tyrosine kinase that is activated by double-stranded DNA-damaging agents, is involved in various signaling pathways, such as proliferation, apoptosis, and DNA repair. (bmbreports.org)
  • overexpression of these genes decreased proliferation or induced apoptosis of human MLL-AF4 + ALL cell lines, respectively. (ashpublications.org)
  • BCR-ABL oncogene activates multiple cross-talking signal transduction pathways (STP), such as RAS/MEK/ERK, PI3K/Akt, Wnt and STAT5, contributing to abnormal proliferation of clonal cells. (oncotarget.com)
  • Considerably, we recently exhibited that Abl kinases are also triggered downstream of deregulated development element receptors (PDGFR, EGFR, IGF-1R, ErbB2/Her-2) and Src family members buy Liquiritin kinases in intrusive breast malignancy cells, and promote invasion, proliferation, and success in response to nutritional deprivation [7, 8]. (researchdataservice.com)
  • Right here, we statement that STI571, an Abl kinase inhibitor, inhibits cell development, proliferation, and induces apoptosis of two cell lines made up of high Abl kinase activity: MDA-MB-435s melanoma cells and MDA-MB-468 breasts cancer cells. (researchdataservice.com)
  • Nevertheless, MTT assays obviously display a dose-dependent in MTT decrease to formazan with STI571 treatment, which is usually inconsistent with proliferation and apoptosis assays. (researchdataservice.com)
  • TRIM13 inhibited cell proliferation and induced cell apoptosis by regulating NF-κB pathway in non-small-cell lung carcinoma cells. (cancerindex.org)
  • Berbamine inhibits proliferation and induces apoptosis of KU812 cells by increasing Smad3 activity[J]. Journal of Zhejiang University Science B, 2011, 12(7): 568-574. (zju.edu.cn)
  • berbamine suppresses KU812 cell proliferation through induction of cell cycle arrest in G 1 and apoptosis . (zju.edu.cn)
  • The PI3K/Akt/mTOR signaling pathway is a key regulator of diverse physiological functions such as proliferation, global protein, and lipid synthesis as well as many metabolic pathways interacting to increase secretory capabilities. (go.jp)
  • The bcr-abl oncoprotein has uncontrolled tyrosine kinase activity, which deregulates cellular proliferation, decreases adherence of leukemia cells to the bone marrow stroma, and protects leukemic cells from normal programmed cell death (apoptosis). (msdmanuals.com)
  • In chronic myelogenous leukemia, the Philadelphia chromosome leads to a fusion protein of abl with bcr (breakpoint cluster region), termed bcr-abl. (keralapharmacist.com)
  • Chromosomal aberrations are commonly associated with inherited chromosomal instabilities, such as the breakpoint cluster region (Bcr). (me.uk)
  • Genes whose protein products stimulate or enhance the division and viability of cells. (cancerquest.org)
  • Genes whose protein products can directly or indirectly prevent cell division or lead to cell death. (cancerquest.org)
  • This domain occurred 415 times on human genes ( 944 proteins). (umbc.edu)
  • The multifunctional regulator nuclear factor erythroid 2-related factor (Nrf2) is considered not only as a cytoprotective factor regulating the expression of genes coding for anti-oxidant, anti-inflammatory and detoxifying proteins, but it is also a powerful modulator of species longevity. (springer.com)
  • The major characteristics of Nrf2 are to some extent mimicked by Nrf2-dependent genes and their proteins including heme oxygenase-1 (HO-1), which besides removing toxic heme, produces biliverdin, iron ions and carbon monoxide. (springer.com)
  • Like Rb protein, many of the proteins encoded by tumor suppressor genes act at specific points in the cell cycle. (medscape.com)
  • TP53 activates the expression of genes involved in apoptosis, cell cycle regulation (p21), and MDM2. (medscape.com)
  • and insertions, inversions and translocations which create fusion genes. (me.uk)
  • Thus, this abnormality can be detected by routine cytogenetics, and the involved genes BCR-ABL1 can be detected by fluorescent in situ hybridization, as well as by PCR. (717698.com)
  • 2nd, we qualitatively examined genes to search for commonality of function amid proteins with high NSAF. (smadpathway.com)
  • Non-receptor tyrosine kinases encoded by the C-ABL GENES. (jefferson.edu)
  • BCR-Abl is the target of selective inhibitors, such as imatinib (Gleevec), used in the treatment of CML. (umbc.edu)
  • Like all tyrosine-kinase inhibitors, imatinib works by preventing a tyrosine kinase enzyme, in this case BCR-Abl, from phosphorylating subsequent proteins and initiating the signaling cascade necessary for cancer development, thus preventing the growth of cancer cells and leading to their death by apoptosis. (keralapharmacist.com)
  • Kaiso and prognosis As expected for a transcriptional aspect, the Kaiso Inhibitors,Modulators,Libraries protein is often discovered while in the nucleus of quite a few tumor or non tumor derived mammalian cell lines. (screeninglibraries.com)
  • Activation of caspases in response to treatment method with Inhibitors,Modulators,Libraries extracts To achieve insights to the potential mechanisms of apoptosis concerned, caspase 3 seven exercise at the same time as pro tein expression of caspase eight and 9 have been measured for that six most potent extracts in HeLa cells just after sixteen h of remedy. (screeninglibraries.com)
  • Imatinib mesylate (IM) and various other BCR-ABL tyrosine kinase inhibitors (TKIs), including dasatinib (DA) and nilotinib (NL), have already been introduced into scientific practice with exceptional therapeutic results on chronic-phase (CP) CML (10C13). (angiogenesis-blog.com)
  • ABL allosteric inhibitors synergize with statins to enhance apoptosis of metastatic lung cancer cells. (inter-publishing.com)
  • Indolizine: In-Silico Identification of Inhibitors against Mutated BCR-ABL Protein of Chronic Myeloid Leukemia. (inter-publishing.com)
  • BCR-ABL tyrosine kinase inhibitors in the treatment of Philadelphia chromosome positive chronic myeloid leukemia: a review. (zju.edu.cn)
  • Cooperativity between ß-agonists and c-Abl inhibitors in regulating airway smooth muscle relaxation. (jefferson.edu)
  • Imatinib also inhibits the abl protein of non-cancer cells but cells normally have additional redundant tyrosine kinases which allow them to continue to function even if abl tyrosine kinase is inhibited. (keralapharmacist.com)
  • The drug selectively inhibits the kinase activity of the BCR ABL fusion protein. (screeninglibraries.com)
  • It is thus concluded that AVM inhibits the activity of BCR/ABL and their subsequent molecular signals, including AKT and MAPK, resulting in cytotoxicity via apoptosis. (spandidos-publications.com)
  • Furthermore to inhibiting BCR-Abl, STI571 also inhibits endogenous c-Abl and Arg [4]. (researchdataservice.com)
  • His scientific interests lie mostly in Signal transduction, Cell biology, Proto-oncogene tyrosine-protein kinase Src, LYN and Cancer research. (research.com)
  • The subject of his Proto-oncogene tyrosine-protein kinase Src research is within the realm of Kinase. (research.com)
  • His primary areas of study are Cell biology, Cancer research, LYN, Proto-oncogene tyrosine-protein kinase Src and Signal transduction. (research.com)
  • Seth J. Corey interconnects Tyrosine kinase, Dasatinib and Receptor tyrosine kinase in the investigation of issues within Proto-oncogene tyrosine-protein kinase Src. (research.com)
  • His LYN study improves the overall literature in Proto-oncogene tyrosine-protein kinase Src. (research.com)
  • Receptor Tyrosine Kinases (RTKs) are a family of tyrosine protein kinases. (callaix.com)
  • Scope includes mutations and abnormal protein expression. (cancerindex.org)
  • This fact explains why many BCR-ABL mutations can cause resistance to imatinib by shifting its equilibrium toward the open or active conformation. (keralapharmacist.com)
  • Nevertheless, early relapses as well as the introduction of IM-resistant disease at any correct period can cause main setbacks for a few sufferers (8,14,15), generally because of the selection and outgrowth of preexisting subclones of cells with mutations in the BCR-ABL kinase area (14,16). (angiogenesis-blog.com)
  • Elimination of BCR/ABL-dependent intracellular signals triggers apoptosis, but it is unclear whether this activates additional cell survival and/or death pathways. (lu.se)
  • IM-induced autophagy did not involve c-Abl or Bcl-2 activity but was associated with ER stress and was suppressed by depletion of intracellular Ca2+, suggesting it is mechanistically. (lu.se)
  • Natural product anticancer agents enhance intracellular levels of ceramide, a sphingolipid that promotes cell apoptosis. (sphingolipidclub.com)
  • Autophagy plays a housekeeping role in removing misfolded or aggregated proteins, removing damaged organelles, eliminating intracellular pathogens. (cancer-research-network.com)
  • Akt1 is also able to induce protein synthesis pathways, and is therefore a key signaling protein in the cellular pathways that lead to skeletal muscle hypertrophy, and general tissue growth. (wikipedia.org)
  • Mixture therapies to focus on various other pathways or proteins, furthermore to BCR-ABL, seem to be far better at inhibiting these cells (28C31). (angiogenesis-blog.com)
  • Proto-Oncogene Proteins c-abl" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (jefferson.edu)
  • This graph shows the total number of publications written about "Proto-Oncogene Proteins c-abl" by people in this website by year, and whether "Proto-Oncogene Proteins c-abl" was a major or minor topic of these publications. (jefferson.edu)
  • Below are the most recent publications written about "Proto-Oncogene Proteins c-abl" by people in Profiles. (jefferson.edu)
  • The Tel-ARG fusion protein, resulting from reciprocal translocation between chromosomes 1 and 12, is associated with acute myeloid leukemia (AML). (umbc.edu)
  • Interestingly, Spautin-1 enhances imatinib mesylate (IM)-induced CML cell apoptosis by reducing the expression of the anti-apoptotic proteins Mcl-1 and Bcl-2. (cancer-research-network.com)
  • Meanwhile, the levels of the anti-apoptotic proteins, such as Bcl-2 and Bcl-xL, were decreased, whereas pro-apoptotic Bax was increased. (zju.edu.cn)
  • The PHLPP isoforms (PH domain and Leucine rich repeat Protein Phosphatases) are a pair of protein phosphatases, PHLPP1 and PHLPP2, that are important regulators of Akt serine-threonine kinases (Akt1, Akt2, Akt3) and conventional/novel protein kinase C (PKC) isoforms. (wikipedia.org)
  • The PTKc family is part of a larger superfamily that includes the catalytic domains of other kinases such as protein serine/threonine kinases, RIO kinases, and phosphoinositide 3-kinase (PI3K). (umbc.edu)
  • Imatinib is quite selective for bcr-abl - it does also inhibit other targets mentioned above (c-kit and PDGF-R), but no other known tyrosine kinases. (keralapharmacist.com)
  • Protein phosphatases play essential roles as negative regulators of kinases and signaling cascades involved in cytoskeletal organization. (cancerbiomed.org)
  • Abl kinase inhibitor) around the viability of malignancy cells containing extremely energetic Abl kinases. (researchdataservice.com)
  • Abl kinases are recognized for their participation in human being leukemia, as c-Abl is usually translocated following to which leads to a BCR-Abl fusion proteins that drives the introduction of persistent myelogenous leukemia (CML) [2]. (researchdataservice.com)
  • AVM induced the release of cleaved PARP and cleaved caspase‑3 caused apoptosis and inhibited the viability of these cells. (spandidos-publications.com)
  • TRIM13-induced NSCLC cell apoptosis was attenuated by a caspase-3 inhibitor Ac-DEVD-CHO, suggesting that TRIM13 induced cell apoptosis partially through a caspase-3-dependent pathway. (cancerindex.org)
  • Catalytic domain of the Protein Tyrosine Kinase, Abelson kinase. (umbc.edu)
  • Imatinib is specific for the TK domain in abl (the Abelson proto-oncogene), c-kit and PDGF-R (platelet-derived growth factor receptor). (keralapharmacist.com)
  • One candidate focus on is certainly Abelson helper integration site 1 (encodes a distinctive proteins with multiple SH3 binding sites, an SH3 area, and seven WD40 repeats, all known mediators of proteinCprotein connections (38). (angiogenesis-blog.com)
  • The resulting BCR-Abl fusion protein is constitutively active and associates into tetramers, resulting in a hyperactive kinase sending a continuous signal. (umbc.edu)
  • As this is now a constitutively active tyrosine kinase, imatinib is used to decrease bcr-abl activity. (keralapharmacist.com)
  • Nrf2 consists of six functional Neh domains (Neh1-Neh6), from which, the amino-terminal Neh2 domain controls binding Keap1-the inhibitor protein Kelch-like ECH-associated protein 1, that is responsible for the cytosolic sequestration of Nrf2 under physiological conditions (Fig. 2 a). (springer.com)
  • Imatinib mesylate (IM), a potent inhibitor of the BCR/ABL tyrosine kinase, has become standard first-line therapy for patients with chronic myeloid leukemia (CML), but the frequency of resistance increases in advancing stages of disease. (lu.se)
  • The p16INK4A protein is a cell-cycle inhibitor that acts by inhibiting activated cyclin D:CDK4/6 complexes, which play a crucial role in the control of the cell cycle by phosphorylating Rb protein. (medscape.com)
  • His LYN research incorporates elements of Molecular biology, Protein kinase B, Cell growth and Syk. (research.com)
  • All molecular weights (MW) are confirmed by comparison to Bio-Rad Rainbow Markers and to western blot mobilities of known proteins with similar MW. (ecmbio.com)
  • Oncogenic transformation of c-abl arises when specific N-terminal amino acids are deleted, releasing the kinase from negative regulation. (jefferson.edu)
  • Recent studies utilizing immunohistochemistry evaluation of ordinary and tumor tissue unveiled that Kaiso protein is predominantly localized inside the cytoplasm in the cell or is totally absent, though. (screeninglibraries.com)
  • 1 probable explanation is the fact that Kaiso, like other proteins or variables that normally reside during the cytoplasm, need a post translational modification, to get targeted and translocated towards the cell nucleus. (screeninglibraries.com)
  • The c-Abl proto-oncogene encodes a nonreceptor type protein tyrosine kinase that is widely expressed and is distributed in both the nucleus and the cytoplasm of cells. (ecmbio.com)
  • 3 Detection of the MLL-AF4 fusion protein in CD34 + /CD19 − fetal hematopoietic stem or progenitor cells or in fetal cells before hematologic specification suggests that there is a window of opportunity during development for the MLL-AF4 fusion protein to immortalize hematopoietic stem and progenitor cells (HSPCs). (ashpublications.org)
  • We have shown here that IM induces autophagy in CML blast crisis cell lines, CML primary cells, and p210BCR/ABL-expressing myeloid precursor cells. (lu.se)
  • We demonstrate here that GSK-3 maintains the MLL leukemia stem cell transcriptional program by promoting the conditional association of CREB and its coactivators TORC and CBP with homedomain protein MEIS1, a critical component of the MLL-subordinate program, which in turn facilitates HOX-mediated transcription and transformation. (stanford.edu)
  • In an earlier study, Barrett et al used a conditional invertor mouse line for cell-specific expression of an Mll-AF4 fusion protein. (ashpublications.org)
  • The CDK4-cyclinD complex normally phosphorylates the retinoblastoma protein (Rb protein), leading to release of the E2F transcription factor and cell cycle progression. (medscape.com)
  • The p19ARF protein, which is encoded by the same locus as p16, also leads to cell cycle arrest by inhibiting the ability of MDM2 to inactivate TP53. (medscape.com)
  • PP2A is involved in diverse regulatory functions, including cell cycle progression, apoptosis, and DNA repair. (cancerbiomed.org)
  • Tripartite Motif Containing 13 (TRIM13), a member of TRIM proteins, is deleted in multiple tumor types, especially in B-cell chronic lymphocytic leukemia and multiple myeloma. (cancerindex.org)
  • We found that TRIM13 mRNA and protein expression was reduced in NSCLC tissues and cell lines in comparison to paired non-cancerous tissues and a human normal bronchial epithelial cell line, respectively. (cancerindex.org)
  • The FIP1-like-1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRα) fusion oncogene is the driver factor in a subset of patients with hypereosinophilic syndrome (HES)/chronic eosinophilic leukemia (CEL). (oncotarget.com)
  • Mixture treatment also statistically considerably improved apoptosis of Compact disc34+ leukemic stem/progenitor cells and removed their long-term leukemia-initiating activity in NSG mice. (angiogenesis-blog.com)
  • Every BCR-ABL1 transcription is concomittant with a specific leukemia phenotype that expects treatment clinical outcome and reaction prognosis. (inter-publishing.com)
  • Polymerase chain reaction -based qualitative and quantitative tests detect and measure the BCR-ABL1RNA transcripts in leukemia cells taken from blood or bone marrow samples. (717698.com)
  • Conclusions Concurrently concentrating on BCR-ABL and JAK2 actions in CML WP1130 (Degrasyn) stem/progenitor cells may improve final results in sufferers destined to build up IM level of resistance. (angiogenesis-blog.com)
  • Specifically, JAK2 bodily interacts using the C-terminal area of BCR-ABL and is among the most prominent goals of BCR-ABL (7,8). (angiogenesis-blog.com)
  • Significantly, AHI-1 bodily interacts with JAK2 and BCR-ABL in CML cells to mediate these natural results, although the type from the direct or indirect interaction between JAK2 and AHI-1 still continues to be uncharacterized. (angiogenesis-blog.com)
  • imatinib) originated to particularly inhibit BCR-Abl, and it is FDA-approved to take care of CML buy Liquiritin [3]. (researchdataservice.com)
  • c-Abl plays a role in normal HEMATOPOIESIS especially of the myeloid lineage. (jefferson.edu)
  • Inhibition of the bcr-abl tyrosine kinase also stimulates its entry in to the nucleus, where it is unable to perform any of its normal anti-apoptopic functions. (keralapharmacist.com)
  • Resistance to imatinib in HES/CEL has been described mainly due to the T674I mutation in FIP1L1-PDGFRα, which is homologous to the imatinib-resistant T315I mutation in BCR-ABL. (oncotarget.com)
  • Additionally, several resistance mechanisms, such as BCR-ABL genomic amplification, are considered ( 4 ). (spandidos-publications.com)
  • The conventional PKCs can be activated by calcium and diacylglycerol, two important mediators of G protein-coupled receptor signaling. (wikipedia.org)
  • Moreover, S116836 induced intrinsic pathway of apoptosis as well as the death receptor pathway, coincided with up-regulation of the proapoptotic BH3-only protein Bim-EL through the Erk1/2 pathway. (oncotarget.com)
  • Ultimately, we compared the volume of proteins and peptides identified from a few technical replicates that used this system to your amount identified by a few common, information dependent technical replicates carried out on the exact samples. (smadpathway.com)
  • Classic anti-cancer strategies aimed at actively killing cancer cells include alkylating agents that generate crosslinks in DNA and trigger repair mechanisms to induce apoptosis, antimetabolites that severely disrupt nucleic acid synthesis, and alkaloids that interfere with microtubule polymerization/depolymerization and halt mitosis 2 . (cancerbiomed.org)
  • As a result, cells expressing different forms of BCR/ABL were recruited for the present study, including K562 (human wild‑type) or TCCY‑T315I (human imatinib‑resistant) and the Ba/F3‑(T315I/E279K/Y253H) (mouse BCR/ABL point mutation‑transfected cells). (spandidos-publications.com)
  • Interestingly, AVM appeared to be more sensitive to imatinib‑resistant (T315I, Y253H, and E279K) than wild‑type BCR/ABL cells, indicating its potential to overcome imatinib‑resistant severe issues in CML. (spandidos-publications.com)
  • Thus, cells expressing different forms of BCR/ABL were recruited for the present study, including K562 [human wild-type (WT)] or TCCY-T315I [human imatinib-resistant (IR)] and the Ba/F3-(T315I/E279K/Y253H) (mouse BCR/ABL point mutation-tranfected cells). (spandidos-publications.com)
  • Imatinib binds to the inactive conformation of the Bcr-Abl TK, occluding its ATP-binding pocket and preventing its switch to the active conformation [10]. (rockstarsagainstliveearth.com)
  • Imatinib works by binding close to the ATP binding site of bcr-abl, locking it in a closed or self-inhibited conformation, and therefore inhibiting the enzyme activity of the protein semi-competitively. (keralapharmacist.com)
  • Involvement of C/EBPβ-related signaling pathway in methamphetamine-induced neuronal autophagy and apoptosis. (cancerindex.org)
  • Our previous study has shown that CCAAT-enhancer binding protein β (C/EBPβ) is an important regulator in METH-induced neuronal autophagy and apoptosis. (cancerindex.org)
  • We hypothesized that C/EBPβ is involved in METH-induced DDIT4-mediated neuronal autophagy and Trib3-mediated neuronal apoptosis. (cancerindex.org)
  • We tested our hypothesis by examining the effects of silencing C/EBPβ, DDIT4, Trib3 or α-syn with small interfering ribonucleic acid (siRNA) on METH-induced autophagy and apoptosis in the human neuroblastoma SH-SY5Y cells. (cancerindex.org)
  • Oxidative stress generated during such stressful conditions may damage DNA and proteins, and as a consequence the cellular processes are disturbed. (springer.com)
  • Ribosomal protein S3 is a protein component of the ribosome, which is a cellular structure that plays a central role in protein synthesis. (bmbreports.org)
  • MDR1 codes for P-glycoprotein (P-gp), a member of the ABC transporter superfamily of proteins that promote cellular efflux of chemotherapeutic agents. (sphingolipidclub.com)
  • When the cellular action(s) is completed, the phosphate group is removed and that protein is "turned off. (callaix.com)
  • Protein enzymes are chains of amino acids and when a phosphoryl group, PO32−, is covalently attached to one of the amino acids, it changes the three-dimensional configuration and function of the protein. (callaix.com)
  • The constantly active BCR-ABL1 protein signals cells to continue dividing abnormally and prevents them from self-destructing, which leads to overproduction of the abnormal cells and, eventually, a shortage of normal blood cells. (medlineplus.gov)
  • PTKs catalyze the transfer of the gamma-phosphoryl group from ATP to tyrosine (tyr) residues in protein substrates. (umbc.edu)
  • Phospho-c-Abl (Tyr-412) synthetic peptide (coupled to KLH) corresponding to amino acid residues around tyrosine 412 of human c-Abl. (ecmbio.com)
  • HO-1 and their products exert beneficial effects through the protection against oxidative injury, regulation of apoptosis, modulation of inflammation as well as contribution to angiogenesis. (springer.com)
  • In this issue of Blood , Malouf et al characterize 2 microRNAs (miRNAs) that are effectors of malignant transformation by the MLL-AF4 fusion protein. (ashpublications.org)
  • CML cells are inherently resistant to apoptosis induced by conventional chemotherapeutic agents. (tcd.ie)
  • Because the BCR-Abl tyrosine kinase enzyme exists only in cancer cells and not in healthy cells, imatinib works as a form of targeted therapy-only cancer cells are killed through the drug's action. (keralapharmacist.com)
  • A variety of stimuli activate c-Abl kinase including integrin activation, PDGF stimulation, and binding to proteins, such as c-Jun. (ecmbio.com)
  • Ribosomal protein S3 (RpS3) is involved in protein biosynthesis as a component of the ribosome complex and possesses endonuclease activity to repair damaged DNA. (bmbreports.org)
  • Latest studies further claim that success and development of primitive CML cells might not also rely on BCR-ABLCTK activity PLAUR (32,33). (angiogenesis-blog.com)
  • This locus, however, also encodes a protein from an alternative reading frame, designated p19ARF. (medscape.com)
  • Abl (or c-Abl) is a ubiquitously-expressed cytoplasmic (or nonreceptor) tyr kinase that contains SH3, SH2, and tyr kinase domains in its N-terminal region, as well as nuclear localization motifs, a putative DNA-binding domain, and F- and G-actin binding domains in its C-terminal tail. (umbc.edu)