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Validated All-in-One™ qPCR Primer for ABL1(NM_007313.3) Search again
Product ID:
HQP149092
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ABL, BCR-ABL, CHDSKM, JTK7, bcr/abl, c-ABL, c-ABL1, p150, v-abl
Gene Description:
ABL proto-oncogene 1, non-receptor tyrosine kinase
Target Gene Accession:
NM_007313.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
The ABL1 protooncogene encodes a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell differentiation, cell division, cell adhesion, and stress response. Activity of c-Abl protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns ABL1 into an oncogene. The t(9;22) translocation results in the head-to-tail fusion of the BCR (MIM:151410) and ABL1 genes present in many cases of chronic myelogeneous leukemia. The DNA-binding activity of the ubiquitously expressed ABL1 tyrosine kinase is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function for ABL1. The ABL1 gene is expressed as either a 6- or 7-kb mRNA transcript, with alternatively spliced first exons spliced to the common exons 2-11. [provided by RefSeq].
Gene References into function
- The abl protein was analyzed by real time quantitative PCR.
- crystal structure of the Bcr-Abl oncoprotein oligomerization domain
- regulates p73 through p38 MAP kinase pathway
- These findings indicate that Rad9 is regulated by a c-Abl-dependent mechanism in the apoptotic response to genotoxic stress. (c-abl protein)
- C terminus of BRCA1 is phosphorylated by c-Abl in vitro (PROTO-ONCOGENE C-ABL)
- Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI571, and they can pre-exist to the onset of treatment.
- This review focuses on how Bcr-Abl affects HSCs and how Bcr-Abl expression alters the properties of HSCs.
- chronic myelogenous leukemia characterized by translocation between chromosomes 9 and 22 forming a BCR-ABL gene, a specific marker for this disease.
- mutations of Tyr-253 in the nucleotide-binding (P) loop of the Abl kinase domain to Phe or His in patients with advanced CML and acquired STI-571 resistance
- The data showed that c-abl expression is differently modified in lymphoid B cell lines.
- Review. ABL protein tyrosine kinases regulate cell proliferation, survival, adhesion, migration, stress responses, and cytoskeletal dynamics.
- determined the NMR solution structure of the ternary complex of the Abl SH3 domain with the Crk SH2 domain bound to a Crk pY221 phosphopeptide
- point mutations in Abl that rendered Bcr-Abl imatinib mesylate-resistant, including a mutation that destabilized the inactive conformation of Abl suggesting that the inhibitor required inactivation of the kinase prior to binding.
- expression of bcr/abl hybridized gene in chronic myeloid leukemia (CML), acute lymphatic leukemia (ALL) and polycythemia vera (PV), and its clinical significance
- Chronic myelocytic leukemia with eosinophilia, t(9;12)(q34;p13), and ETV6-ABL gene rearrangement: case report and review of the literature.
- An inherited, apparently balanced translocation involving chromosomes 3(q22), 22(q12), and 9(q34.1, resulting from meiotic recombination, leads to deletion in the ABL gene in a child with axial hypotonia and dysmorphism. )
- constitutively activated Bcr-Abl kinase pathways in primitive CML progenitors cooperate with growth factors producing a growth response and disrupt the normally required synergistic interactions between kit ligand and other cytokines to achieve activatio
- concluded that the IRS-1 protein is involved in the signalling pathway of the BCR-ABL tyrosine kinase
- detection of kinase domain mutations was almost always associated with imatinib resistance, and patients with mutations in the P-loop had a particularly poor prognosis
- In conclusion, effective and prompt IR-induced Rad51 focus formation is cell cycle-regulated and requires both ATM and c-Abl.
- This gene is regulated by a myristoyl/phosphotyrosine switch.
- mechanism by which caspases can recruit c-Abl to the nuclear compartment and to the mammalian apoptotic program
- c-Abl-mediated phosphorylation of Mena is regulated by Abi-1
- BCR-ABL is inhibited by lyp tyrosine phosphatase
- Dok-R and c-Abl interact in both a constitutive and inducible fashion and Dok-R influences the intracellular kinase and biological activity of c-Abl
- c-Abl and Arg regulate catalase and that this signaling pathway is of importance to apoptosis in the oxidative stress response
- BCR/ABL amplification may play a role as a novel mechanism in the progression to an aggressive blast transformation in some cases of Philadelphia chromosome-positive chronic myelocytic leukemia
- c-Abl increases the cellular p73 abundance through posttranslational regulation. Kinase activity is essential for c-Abl to up-regulate p73. c-Abl contributes to either pro- or antiapoptotic process depending on the expression profile of p73 isoforms.
- c-Abl tyrosine kinase selectively regulates p73 nuclear matrix association
- Expression of BCR/ABL and BCL-2 in myeloid progenitors leads to myeloid leukemias.
- ABL-kinase domain point mutation as a cause of imatinib resistance in CML patient who progress to myeloid blast crisis
- differential utilization of the p53 and c-Abl/p73 pathways by different tumor cell line.
- we have identified a direct binding between WRN and c-Abl in vitro via the N-terminal and central regions of WRN and the Src homology domain 3 of c-Abl. These findings suggest a novel signaling pathway
- findings indicate that, in addition to stimulating catalase activity, c-Abl and Arg promote catalase degradation in the oxidative stress response
- The deletion of the 5'abl region on der(9), present in approximately 9% of the CML, takes place at the same time as the formation of the Ph chromosome translocation and seems of worse prognosis
- the equilibrium fraction of c-Abl in which the myristoylated N-terminal is unlatched is approximately 0.5%
- ABL fuses with BCR to form a fusion protein.
- down-regulation of Bcr-Abl mRNA might be one of the mechanisms implicated in the apicidin-mediated apoptosis in the K562 cells
- Describe RT-PCR/capillary electrophoresis method for quantification of bcr-abl transcripts in leukemia.
- Bcr-Abl-mediated transformation involves transcriptional activation of the PKCiota gene, which in turn is required for Bcr-Abl-mediated chemoresistance
- results confirm the high frequency of BCR-ABL kinase domain mutations in patients with secondary resistance to imatinib and exclude mutations of the activation loops of KIT, PDGFRA and PDGFRB as causes of resistance in patients without ABL mutations
- bcr-abl transcript can be detected in the PBLs of Philadelphia chromosome (Ph)-negative essential thrombocythemia but the level of expression is markedly less than that in CML
- BCR-ABL1 kinase activity is linked to defective pre-B cell receptor signaling
- NUP214-ABL1 expression defines a new subgroup of individuals with T-ALL
- FISH analysis of the abl and bcr genes showed the signal for bcr/abl fusion on the der(22) chromosome but not on the der(9) chromosome in Philadelpha-Negative chronic myeloid leukemia.
- Bcr-Abl mediates protection from apoptosis downstream of mitochondrial cytochrome c release
- Abl is a prototype of oncogenic fusion proteins in chronic myeloid leukemia [review]
- Abi enhances Abl-mediated downregulation and phosphorylation of Cdc2 kinase
- the ability to regulate the cellular abundance of mitogen-activated protein kinase 7 contributes to the oncogenic potential of Abl kinases
- MCL-1 is a BCR/ABL-dependent survival factor and interesting target in chronic myeloid leukemia.
- caspase-9 autoprocessing is regulated by c-Abl in the apoptotic response to genotoxic stress.
- Abi-1-mediated coupling of Abl to WAVE2 promotes Abl-evoked WAVE2 tyrosine phosphorylation required to link WAVE2 with activated Rac and with actin polymerization and remodeling at the cell periphery.
- the promoter specificity plays an important role in selective activation of p53 DNA binding by c-Abl
- c-Abl has a role in the DNA-damage stress response and in cell physiology (review)
- JNK phosphorylates 14-3-3 proteins, which regulate nuclear targeting of c-Abl in the apoptotic response to DNA damage
- the incidence of deletions from the der(9) in childhood acute lymphoblastic leukemia is at least as high as that reported for chronic myeloid leukemia.
- Along with BCR, deleted in leukemia, myeloid, philadelphia-positive.
- Bcr-Abl-induced abnormalities in glucose transport regulation have roles in chronic myeloid leukaemia
- ability of Bcr-Abl to stimulate the expression of osteopontin
- TopBP1 is a c-Abl-interacting protein and a repressor for c-Abl expression
- Tyr-394 is the main residue for Abl phosphorylation of tau. Abl is seen in pretangle brain neurons from Alzheimer cases. phosphorylation of tau on Tyr-394 is is potentially part of a signal relay. Abl could have a pathogenic role in Alzheimer's disease.
- c-Abl promotes the induction of EGR1 through the MEK/ERK pathway in regulating apoptotic response to oxidative stress.
- A mechanism for how Crk-II functions in the transactivation of the Abl tyrosine kinase.
- BCR-ABL1 induces aberrant splicing of IKAROS, which interferes with lineage identity and differentiation of pre-B lymphoblastic leukemia cells.
- The TCR gene rearrangements in childhood B-lineage acute lymphoblastic leukemia was associated with expression of bcr/abl chimeric oncogene.
- activation of the c-Abl-PKCdelta-Rac1-p38 MAPK pathway in response to ionizing radiation signals conformational changes of Bak and Bax, resulting in mitochondrial activation-mediated apoptotic cell death in human non-small cell lung cancer cells
- The choronic myeloid leukemia(CML) derived MSCs did not express BCR/ABL gene and Ph chromosome, and had not the ability to development tumor in nude mice. At last, they could express hematopoietic cytokines, and possessed hematopoietic supportive ability
- Small-angle X-ray scattering (SAXS) analysis shows that a mutated form of c-Abl, in which the N-terminal cap and two other key contacts in the autoinhibited state are deleted, exists in an extended array of the SH3, SH2, and kinase domains.
- The results could be considered as an evidence of an actual biological phenomenon that could provide additional information about the Fusion Proteins, bcr-abl and HOXA9 role in the CML progression.
- Data show that nuclear accumulations of p53 and Mdm2 are accompanied by reductions in c-Abl and p300 in zinc-depleted human hepatoblastoma cells.
- The present study demonstrates that c-Abl and Arg (abl-related gene) tyrosine kinases associate with and phosphorylate the proteasome PSMA7 (alpha4) subunit at Tyr-153.
- c-Abl represents a target downstream of phosphatidylinositol 3-kinase-activated PAK2, which differentiates TGF-beta signaling in fibroblasts and epithelial cell lines.
- c-Abl activates WAVE2 via tyrosine phosphorylation to promote actin remodeling in vivo; Abi-1 forms the crucial link between these two factors
- the Bcr-Abl SH3-SH2 region is phosphorylated by Src family kinases, which modulate Bcr-Abl transforming activity
- retention of a dephosphorylated p210Bcr-Abl has a biologic impact distinct from that of downregulation/loss of p210Bcr-Abl and, in a subset of patients, loss of the target of the kinase inhibitor may lead to imatinib mesylate resistance
- BCR-ABL-expressing leukemic stem cells depend to a greater extent on CD44 for homing and engraftment than do normal hematopoietic stem cells
- NESH (Abi-3), like Abi-1 and Abi-2, is a component of the Abi/WAVE complex, but likely plays a different role in the regulation of c-Abl.
- These results suggest an important role of tyrosine 311 in the apoptotic function of PKCdelta and implicate c-Abl as the kinase that phosphorylates this tyrosine.
- Upon H. pylori infection c-Abl directly interacts with CagA and localizes in focal adhesion complexes and membrane ruffles, which are highly dynamic cytoskeletal structures necessary for cell motility
- a system akin to the BCR-ABL translocation of CML may be involved in genomic instability in about one-third of colorectal carcinomas
- The interaction between c-Cbl and SLAP in v-Abl-3T3 cells positively influenced c-Cbl-mediated spreading and adhesion of these cells
- BCR-ABL-kinase domain mutations in patients with a stable CCR are infrequent, and their detection does not consistently predict relapse. Alternative mechanisms must be responsible for disease persistence in the majority of patients.
- Fusion transcription in 16 year old girl with chronic myeloid leukemia.
- BCR-ABL mutations confer resistance to the Abl kinase inhibitor AMN107 (nilotinib) in chronic myeloid leukemia
- overexpression of c-Abl tyrosine kinase activated p21 promoter and endogenous p21 transcription in U2OS cells.
- Bcr-Abl overexpression results in increased proliferation and antiapoptotic signaling in CD34(+) cells, but may not play a direct role in imatinib resistance in progenitor cells expressing either wild-type or mutant BCR/ABL genes.
- The expression of Bcr-Abl leads to hyper-responsiveness of myeloid cells to TGFbeta; this novel cross-regulatory mechanism might play an important role in maintaining the transformed progenitor cell population in CML.
- conclude that our patient represents another case of the rare hematological entity characterized by an ETV6-ABL translocation
- Ubp43 deficiency increases the resistance to oncogenic transformation by BCR-ABL
- Acute myelogenous leukemia patients respond to imatinib mesylate only when BCR-ABLE kinase is inhibited.
- Primary and cultured chronic myeloid leukemia stem cellsdisplay instability of the BCR-ABL fusion gene both in vivo and in vitro.
- Oncogenic activation of c-Abl due to lack of FUS1 expressionin results in non-small cell lung cancer.
- ERF is targeted for inactivation by transforming oncogenes such as vAbl.
- CapZIP is fused to ABL1 in a t(1;9)(q24;q34)-associated B-cell acute lymphoblastic leukemia
- alternatively spliced transcripts lacking exon 7 in c-abl gene were associated with resistance to imatinib
- T-cell repertoire of a patient with chronic myeloid leukemia in major molecular remission due to imatinib mesylate was also dominated by T cells directed against Bcr-Abl-regulated antigens
- Results show that by activating Abl-1 signalling pathway, Anaplasma phagocytophilum protein AnkA facilitates its intracellular infection.
- p210BCR-ABL oncoprotein activity is linked to centrosomal hypertrophy
- BCR/ABL induces SPK1 expression and increases its cellular activity, leading to upregulation of Mcl-1 in CML cells.
- These results indicate that long-term pre-treatment with Docosahexaenoic acid makes Bcr-Abl HL-60 cells more susceptible to the toxic effect of imatinib.
- c-Abl activation by insulin, via a modification of FAK response, may play an important role in directing mitogenic versus metabolic insulin receptor signaling.
- the activation of WAVE3 to promote actin remodeling is enhanced by the c-Abl-mediated tyrosine phosphorylation of WAVE3.
- BCR/ABL-Y177 plays an essential role in Ras and Akt activation and in human hematopoietic progenitor transformation in chronic myelogenous leukemia
- c-Abl may determine cell fate via its subcellular localization [review]
- suggest a role for a combination of ABL kinase inhibitors, perhaps including VX-680, to prevent the outgrowth of cells harboring drug-resistant BCR-ABL mutations
- A role for ARF in human Philadelphia chromosome-positive lymphoblastic leukemia progression.
- The incidence of BCR-ABL fusion oncogene in Pakistani patients with childhood acute lymphoid leukemia is diferent from other populations.
- Significant percentage of the total endogenous Crk II partitions in the nucleus in mammalian cells, where it forms distinct complexes with DOCK180, Wee1, and Abl.
- Imatinib mesylate-resistant chronic myelogenous leukemia patients harbor T315I BCR-ABL mutation
- Crystal structure of the T315I Abl mutant in complex with the aurora kinases inhibitor PHA-739358.
- mutations in BCR-ABL causing resistance to both Imatinib Mesylate and Dasatinib in a chronic myeloid leukaemia patient is associated with lymphoid blast crisis
- p38 MAPK activation in response to cisplatin does not require the tyrosine kinase activity of c-Abl
- requirement of E2F3 for BCR/ABL leukemogenesis
- by activating the Abi1 pathway, Bcr-Abl induces a translocation of MT1-MMP to a membrane-associated structural complex enriched with F-actin and adhesion molecules.
- concurrent JAK2V617F and BCR-ABL translocation appeared to affect independent subclones
- two cases described here presented a masked t(9;22)(q34;q11.2) in association with a t(19;21); in both cases, the masked Philadelphia chromosome resulted from an insertion of ABL in 22q11, with a proven 22q deletion in one case
- p210(BCR-ABL) is arranged in discrete foci in the cytoplasm of cell lines and primary CD34(+) cells but not mononuclear cells suggesting the foci may be a feature of immature chronic myeloid leukaemia cells.
- These results demonstrate that allele-specific changes in gene expression, with selective, progressive silencing of the wild-type ABL1 allele in favor of the oncogenic BCR-ABL1 allele occur in CML patients with therapy-resistant disease.
- MUC1 stabilizes Bcr-Abl and contributes to pathogenesis of chronic myelogenous leukemia cells by promoting self renewal and the MUC1 cytoplasmic domain.
- Phosphorylation of c-Abl by Pak2 inhibits the interaction between the SH3 domain of Abi2 and the PxxP motif of c-Abl, and the phosphorylation enhances the association of c-Abl with the substrate Crk and increases c-Abl-mediated phosphorylation of Crk.
- Up-regulation, in contrast to activation, of the ubiquitously expressed Src kinase, Fyn, by BCR-ABL1, is described.
- novel and complex Ph-negative chronic myeloid leukemia case in which the BCR/ABL protein is located on 3p14.
- BCR-ABL impairs host defenses and promotes malignant transformation, involving dual suppression of IFN-activated signaling pathways
- identify c-Abl as a key player in the signaling cascade, leading to actin reorganization during T-cell activation
- dynamics of ABL1 kinase mutations in BCR-ABL1
- BCR-ABL1 in malignant cells constitutively increases expression of activation-dependent epitopes of LFA-1 and complete loss of responsiveness of LFA-1 to SDF-1-induced "inside-out" signaling involving CXCR4 and Lyn, leading to aberrant adhesive responses
- pharmacological inhibition of c-Abl compromises DNA-damage response
- results demonstrate that PDGFRbeta and Abl kinases function redundantly to promote efficient uptake of Chlamydia trachomatis
- activated c-Abl tyrosine kinase, not as a fusion protein, plays an important role in malignant solid tumors of lung and breast.
- SphK1 is a downstream effector of the Bcr-Abl/Ras/ERK pathway
- ABL1 deletions are not associated with the complexity of translocation genesis of chronic myeloid leukemia
- BCR/ABL kinase abrogates mismatch repair activity to inhibit apoptosis and induce mutator phenotype.
- c-Abl tyrosine kinase per se may be a negative regulator of growth factor signaling.
- MMR-dependent intrinsic apoptosis is p53-independent, but stimulated by hMLH1/c-Abl/p73alpha/GADD45alpha retrograde signaling
- c-Abl kinase has a role in DNA mismatch repair-dependent G2 cell cycle checkpoint arrest responses
- c-Abl and Cdk5 cooperatively regulate maximal activation of p53, resulting in neuronal death in response to oxidative stress by hydrogen peroxide.
- Expression of miR-203 reduces ABL1 and BCR-ABL1 fusion protein levels and inhibits tumor cell proliferation in an ABL1-dependent manner, suggesting it may function as a tumor suppressor.
- mediates intracellular signals to regulate a variety of cellular responses and its genomic mutations and alterations underlie cancer, viral and/or bacterial infections.[review]
- Novel point mutations should be confirmed by analyzing the normal ABL alleles to exclude polymorphisms
- nuclear c-Abl kinase can activate CSF-1 gene transcription by regulating AP-1 activity in the signaling events induced by L-selectin ligation.
- ABL kinase domain pseudoexon insertion is not uncommon in BCR-ABL transcripts.
- BCR-ABL leukemogenesis inis blocked by PI3K in mice, and a dual PI3K/mTOR inhibitor prevents expansion of human BCR-ABL+ leukemia cells
- These results demonstrate regulated tyrosine phosphorylation of AIB1/SRC-3 at a C-terminal tyrosine residue (Y1357) that is phosphorylated after insulin-like growth factor 1, epidermal growth factor, or estrogen treatment of breast cancer cells.
- c-Abl and D40 interact with the tumor suppressor pRb protein and subsequently can lead to regulation of the cell proliferation.
- The SH2 and catalytic domains of active Fes and Abl pro-oncogenic kinases form integrated structures essential for effective tyrosine kinase signaling.
- a thorough biochemical comparative analysis of NUP214-ABL1 and BCR-ABL1 show that, despite their common tyrosine kinase domain, the two fusion proteins differ in many critical catalytic properties
- Hck has a nonredundant function as a key downstream signaling partner for Bcr-Abl and may represent a potential drug target in CML
- Results identify a mechanism by which the WAVE2 complex regulates T cell receptor signaling to Rap1 and integrin activation via Abl- and CrkL-C3G.
- Taken together, these findings indicate that c-Abl is activated during S. enterica serovar Typhimurium infection and that its phosphorylation of multiple downstream targets is functionally important in bacterial internalization.
- Rap1 as another downstream target of the Abl-CrkII signaling module and show that Abl-CrkII collaborates with Rho-ROCK1 to stimulate cell retraction.
- inhibition of EGFR endocytosis occurs via a CagA-dependent activation of the non-receptor kinase c-Abl, which in turn phosphorylates the EGFR target site pY1173.
- BCR/ABL enhances the accumulation of DSBs and alters the apoptotic threshold in CML leading to error-prone DNA repair
- detection of Bcr/Abl transcripts in newly diagnosed chronic myelogenous leukemia cases
- c-Abl and p53 are important for execution of the cell death program initiated in A2E-laden RPE cells exposed to blue light, while JNK might play an anti-apoptotic role
- BCR-ABL inhibition is sufficient to commit chronic myeloid leukemia cells irreversibly to apoptosis