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Journal articles on the topic 'Abl2'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

Zhang, Ke, Wanqing Lyu, Ji Yu, and Anthony J. Koleske. "Abl2 is recruited to ventral actin waves through cytoskeletal interactions to promote lamellipodium extension." Molecular Biology of the Cell 29, no. 23 (November 15, 2018): 2863–73. http://dx.doi.org/10.1091/mbc.e18-01-0044.

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Abl family nonreceptor tyrosine kinases regulate changes in cell shape and migration. Abl2 localizes to dynamic actin-rich protrusions, such as lamellipodia in fibroblasts and dendritic spines in neurons. Abl2 interactions with cortactin, an actin filament stabilizer, are crucial for the formation and stability of actin-rich structures, but Abl2:cortactin-positive structures have not been characterized with high spatiotemporal resolution in cells. Using total internal reflection fluorescence microscopy, we demonstrate that Abl2 colocalizes with cortactin at wave-like structures within lamellum and lamellipodium tips. Abl2 and cortactin within waves are focal and transient, extend to the outer edge of lamella, and serve as the base for lamellipodia protrusions. Abl2-positive foci colocalize with integrin β3 and paxillin, adhesive markers of the lamellum–lamellipodium interface. Cortactin-positive waves still form in Abl2 knockout cells, but the lamellipodium size is significantly reduced. This deficiency is restored following Abl2 reexpression. Complementation analyses revealed that the Abl2 C-terminal half, which contains domains that bind actin and microtubules, is necessary and sufficient for recruitment to the wave-like structures and to support normal lamellipodium size, while the kinase domain–containing N-terminal half does not impact lamellipodium size. Together, this work demonstrates that Abl2 is recruited with cortactin to actin waves through cytoskeletal interactions to promote lamellipodium extension.

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2

Zhang, Gaolian, Meng Xia, Jianhui Guo, Yi Huang, Jianrong Huang, Kecong Wei, Xiaoning Zhang, Jing Zeng, and Weibin Liang. "microRNA-1296 Inhibits Glioma Cell Growth by Targeting ABL2." Technology in Cancer Research & Treatment 20 (January 1, 2021): 153303382199000. http://dx.doi.org/10.1177/1533033821990009.

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Aberrant expression of microRNAs (miRNAs) has been reported to play a role in tumorigenesis. Dysfunction of miR-1296 was found in a variety of cancers, however, the function of miR-1296 in the progression of glioma remains largely understood. Here, our results showed that miR-1296 was significantly down-regulated in glioma tissues and cell lines. Decreased expression of miR-1296 was associated with the tumor size, WHO grade and karnofsky performance scale (KPS) of glioma patients. Low expression of miR-1296 was significantly correlated with the shorter 5-year overall survival of glioma patients. Overexpression of miR-1296 inhibited the proliferation, colony formation, migration and induced apoptosis of glioma cells. MiR-1296 was found to bind the 3’-untranslated region (UTR) of ABL proto-oncogene 2 (ABL2) and subsequently repressed both the mRNA and protein expression of ABL2. ABL2 was overexpressed in glioma tissues and inversely correlated with that of miR-1296. Ectopic expressed ABL2 could reverse the inhibitory effects of miR-1296 on glioma cell proliferation. Our results illustrated the novel tumor-suppressive function of miR-1296 in glioma via repressing ABL2, suggesting a potential application of miR-1296 in the treatment of glioma.

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Pendergast, Ann Marie, Jacob Hoj, and Benjamin Mayro. "BSCI-05. ABL2-HSF1-E2F signaling axis promotes lung adenocarcinoma brain metastasis." Neuro-Oncology Advances 3, Supplement_3 (August 1, 2021): iii2. http://dx.doi.org/10.1093/noajnl/vdab071.004.

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Abstract Brain metastases are the most common intracranial tumors in adults and are associated with increased patient morbidity and mortality. Limited therapeutic options are currently available for the treatment of brain metastasis. We have identified an actionable signaling pathway utilized by metastatic tumor cells whereby the transcriptional regulator Heat Shock Factor 1 (HSF1) drives a transcriptional program, divergent from its canonical role as the master regulator of the heat shock response, leading to enhanced expression of a subset of E2F transcription factor family gene targets. We showed that HSF1 is required for survival and outgrowth by metastatic lung cancer cells in the brain parenchyma. Unexpectedly, we identified the ABL2 tyrosine kinase as an upstream regulator of HSF1 protein expression, and showed that the Src-homology 3 (SH3) domain of ABL2 directly interacts with HSF1 protein at a non-canonical, proline-independent SH3 interaction motif. Importantly, knockdown of ABL2 impairs expression of HSF1 protein and HSF1-E2F transcriptional gene targets. Notably, we found that pharmacologic inhibition of the ABL kinases using selective ABL allosteric inhibitors, but not ATP-competitive inhibitors, ablates the physical interaction between ABL2 and HSF1, leading to markedly decreased expression of HSF1, E2F1 and E2F8 proteins in brain-metastatic lung cancer cells, and depletion of HSF1-E2F transcriptional targets. These findings highlight potential differences affecting intra- and inter-molecular protein-protein interactions induced by allosteric versus ATP-competitive kinase inhibitors that have important therapeutic implications. Importantly, the targetable nature of the ABL2-HSF1-E2F signaling network identifies ABL allosteric inhibitors as a potentially effective therapy for the treatment of metastatic lung cancers characterized by high expression of HSF1.

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Hoj, Jacob P., Benjamin Mayro, and Ann Marie Pendergast. "The ABL2 kinase regulates an HSF1-dependent transcriptional program required for lung adenocarcinoma brain metastasis." Proceedings of the National Academy of Sciences 117, no. 52 (December 14, 2020): 33486–95. http://dx.doi.org/10.1073/pnas.2007991117.

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Brain metastases are the most common intracranial tumors in adults and are associated with increased patient morbidity and mortality. Limited therapeutic options are currently available for the treatment of brain metastasis. Here, we report on the discovery of an actionable signaling pathway utilized by metastatic tumor cells whereby the transcriptional regulator Heat Shock Factor 1 (HSF1) drives a transcriptional program, divergent from its canonical role as the master regulator of the heat shock response, leading to enhanced expression of a subset of E2F transcription factor family gene targets. We find that HSF1 is required for survival and outgrowth by metastatic lung cancer cells in the brain parenchyma. Further, we identify the ABL2 tyrosine kinase as an upstream regulator of HSF1 protein expression and show that the Src-homology 3 (SH3) domain of ABL2 directly interacts with HSF1 protein at a noncanonical, proline-independent SH3 interaction motif. Pharmacologic inhibition of the ABL2 kinase using small molecule allosteric inhibitors, but not ATP-competitive inhibitors, disrupts this interaction. Importantly, knockdown as well as pharmacologic inhibition of ABL2 using allosteric inhibitors impairs expression of HSF1 protein and HSF1-E2F transcriptional gene targets. Collectively, these findings reveal a targetable ABL2-HSF1-E2F signaling pathway required for survival by brain-metastatic tumor cells.

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Hu, Yuhan, Wanqing Lyu, Laura Anne Lowery, and Anthony J. Koleske. "Regulation of MT dynamics via direct binding of an Abl family kinase." Journal of Cell Biology 218, no. 12 (November 7, 2019): 3986–97. http://dx.doi.org/10.1083/jcb.201812144.

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Abl family kinases are essential regulators of cell shape and movement. Genetic studies revealed functional interactions between Abl kinases and microtubules (MTs), but the mechanism by which Abl family kinases regulate MTs remains unclear. Here, we report that Abl2 directly binds to MTs and regulates MT behaviors. Abl2 uses its C-terminal half to bind MTs, an interaction mediated in part through electrostatic binding to tubulin C-terminal tails. Using purified proteins, we found that Abl2 binds growing MTs and promotes MT polymerization and stability. In cells, knockout of Abl2 significantly impairs MT growth, and this defect can be rescued via reexpression of Abl2. Stable reexpression of an Abl2 fragment containing the MT-binding domain alone was sufficient to restore MT growth at the cell edge. These results show Abl2 uses its C-terminal half to bind MTs and directly regulate MT dynamics.

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6

Thompson, Eric, Jill Jones, Reb Kornaherns, and Steven Zhang. "CSIG-32. ABL1 AND 2 DRIVE MEDULLOBLASTOMA PROLIFERATION AND ADHESION IN LEPTOMENINGEAL DISSEMINATION." Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii46. http://dx.doi.org/10.1093/neuonc/noac209.181.

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Abstract INTRODUCTION The molecular mechanisms that drive leptomeningeal dissemination (LD) of medulloblastoma (MB) are largely unknown. The Abelson (ABL) family kinases, originally identified as oncogenes in leukemia, play an important role in lung cancer cell migration, invasion, cell adhesion, and chemotherapy resistance. The objective of this work was to elucidate the role of ABL kinases in MB LD. METHODS ABL1 and ABL2 mRNA expression of patient specimens was analyzed. shRNA knockdowns of ABL1/2 and pharmacologic inhibition of ABL1/2 were used for in vitro and in vivo analyses of MB LD. RESULTS ABL1 and ABL2 levels were significantly higher in MB patients with LD than without (p=2.6x10-10 and 7.2x10-7, respectively) and overall survival was significantly reduced in patients with high ABL1 and 2 expression (p=0.019 and 0.00027, respectively). In vitro pharmacologic inhibition and genetic knockdown of ABL1 and ABL2 in Group 3/4 MB resulted in statistically significant cell death, decreased adhesion to vitronectin (a key leptomeningeal extracellular matrix [ECM] protein), decreased migration through ECM extract, and decreased c-myc expression in multiple MB cell types. In mouse models of MB LD, ABL1/2 knockdown significantly decreased LD as determined by bioluminescence and improved overall survival (p=0.0044). Pharmacologic inhibition of ABL1/2 using nilotinib resulted in improved median overall survival (64 vs. 76.5 days). CONCLUSIONS ABL1 and ABL2 are preferentially expressed in patients with MB LD at diagnosis and are associated with poor survival. Both genetic inactivation and pharmacologic inhibition of ABL1 and 2 decreased MB LD in vitro and in vivo, likely via reduction of c-myc signaling. This preliminary work suggests a key role for ABL1/2 in driving MB LD.

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7

Duan, Daisy, Wanqing Lyu, and Tony Koleske. "Elucidating how Abl2 tyrosine kinase regulates microtubule dynamics." Biophysical Journal 121, no. 3 (February 2022): 115a—116a. http://dx.doi.org/10.1016/j.bpj.2021.11.2155.

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8

Roberts, Kathryn G., Yung-Li Yang, Debbie Payne-Turner, Richard C. Harvey, I.-Ming Chen, Shalini C. Reshmi, Gastier-Foster Julie, et al. "Functional Analysis of Kinase-Activating Fusions in Ph-like Acute Lymphoblastic Leukemia." Blood 124, no. 21 (December 6, 2014): 786. http://dx.doi.org/10.1182/blood.v124.21.786.786.

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Abstract Introduction: Ph-like or BCR-ABL1-like B-progenitor acute lymphoblastic leukemia (ALL) is a high-risk subtype characterized by a gene expression profile similar to BCR-ABL1 ALL. The prevalence of Ph-like ALL rises from 10% in standard risk childhood ALL to over 25% in young adults. Next-generation sequencing of Ph-like ALL identified a variety of alterations involving kinase or cytokine receptor genes, including rearrangement, sequence mutation and copy number alterations. Chromosomal rearrangements in about one-third of Ph-like ALL cases create fusion genes of a variety of 5’ partners that involve ABL1-class genes (ABL1, ABL2, CSF1R and PDGFRB) or activate JAK family members (JAK2, TYK2, IL2RB) that are potentially amenable to treatment with ABL1-class or JAK-class tyrosine kinase inhibitors (TKIs). Notably, ABL2 (Abelson-related gene, ARG), a homolog of ABL1, has rarely been identified as a rearrangement partner in ALL. CSF1R (encoding the macrophage colony stimulating receptor) regulates the differentiation of macrophages, and is not normally expressed in lymphocytes. Likewise, rearrangements involving the JAK family member TYK2, the beta chain of the interleukin 2 cytokine receptor (IL2RB), and the neurotrophic tyrosine kinase receptor type 3 (NTRK3), have not been previously described in leukemia. The goals of this study were to assess the role of these kinase alterations in leukemogenesis, to determine the activation of signaling pathways, and to investigate the efficacy of TKIs. Methods: Kinase fusions were expressed in interleukin-3 dependent Ba/F3 cells, and co-expressed with the dominant negative isoform of IKAROS (IK6) in interleukin-7 dependent Arf-/- mouse pre-B cells. Xenograft models of 10 Ph-like ALL tumors - ETV6-ABL1, RANBP2-ABL1, PAG1-ABL2, RCSD1-ABL2, SSBP2-CSF1R, IGH-EPOR, ETV6-NTRK3, ATF7IP-JAK2, PAX5-JAK2 and ZEB2-PDGFRB - were generated by engrafting primary human leukemia cells into NOD-SCID IL2R gamma null (NSG) mice. Activation of kinase signaling was performed using phosphoflow cytometry analysis, and sensitivity to TKIs was assessed ex vivo and in vivo. Results: All kinase fusions (PAG1-ABL2, MYH9-IL2RB, ATF7IP-JAK2, ETV6-NTRK3 or MYB-TYK2) induced cytokine-independent proliferation of Ba/F3 cells. Mice transplanted with Arf-/- pre-B cells co-expressing IK6 and either RCSD1-ABL2 or SSBP2-CSF1R developed pre-B ALL (CD43+, B220+, CD19+, BP-1+ and IgM-) with a median latency of 36 and 40 days respectively, providing evidence that ABL2 and CSF1R fusions contribute to leukemogenesis. In human leukemic cells harvested from xenograft mice we observed distinct patterns of kinase signaling activation and TKI sensitivity for the different fusions. Xenograft cells expressing ABL1-class kinase fusions showed activation of STAT5 that was inhibited with imatinib or dasatinib. Phosphorylation of CRKL, a known target of ABL1 and ABL2, was only observed in cells expressing ABL1/2 fusions. Cells harboring ATF7IP-JAK2, PAX5-JAK2 or IGH-EPOR showed phosphorylation of STAT5 that was attenuated with the JAK2 inhibitor, ruxolitinib. In contrast, cells expressing ETV6-NTRK3 signaled through the MAPK pathway with constitutive pERK1/2 that was inhibited with the ALK-inhibitor, crizotinib. This TKI response profile was confirmed by cytotoxicity assays in xenograft cells, with ABL1-class fusions being sensitive to dasatinib (IC50 range 1-2nM), whilst cases harboring ATF7IP-JAK2 or EPOR rearrangement uniquely responded to ruxolitinib with IC50 values of 500nM and 850nM respectively. Interestingly, in human leukemic cells harboring the ETV6-NTRK3 fusion we observed selective inhibition with both crizotinib and the FLT3 inhibitor, lestaurtinib. Pre-clinical studies on three xenograft models of Ph-like ALL - ETV6-ABL1, RCSD1-ABL2 and SSBP2-CSF1R – showed significantly reduced leukemic burden in dasatinib treated mice (20mg/kg/day p.o) compared to vehicle treated mice. Conclusions: These data provide important insight on new targets of rearrangement in ALL and describe the first engineered mouse models of Ph-like B-ALL. Functional modeling of these alterations is essential to improve the clinical management of Ph-like ALL by identifying patients with specific genomic lesions at diagnosis and directing them to treatment with appropriate TKIs combined with chemotherapy, analogous to current treatment for BCR-ABL1 B-ALL. Disclosures Hunger: Bristol Myers Squibb: Consultancy.

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9

Tremblay, Matthew, and Peter Davies. "P3-330: Tyrosine phosphorylation of tau by Abl2 (ARG)." Alzheimer's & Dementia 2 (July 2006): S471—S472. http://dx.doi.org/10.1016/j.jalz.2006.05.1600.

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10

Liu, Yun, Chen Shao, Linqi Zhu, Sihong Jiang, Guanlin Li, Wei Zhang, Yajing Lin, Ying Ni, Hui Cao, and Shihe Shao. "High Expression of ABL2 Suppresses Apoptosis in Gastric Cancer." Digestive Diseases and Sciences 63, no. 9 (May 16, 2018): 2294–300. http://dx.doi.org/10.1007/s10620-018-5111-7.

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11

Thines, Louise, Zhigang Li, and David B. Sacks. "IQGAP1 Is a Phosphotyrosine-Regulated Scaffold for SH2-Containing Proteins." Cells 12, no. 3 (February 2, 2023): 483. http://dx.doi.org/10.3390/cells12030483.

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The scaffold protein IQGAP1 associates with over 150 interactors to influence multiple biological processes. The molecular mechanisms that underly spatial and temporal regulation of these interactions, which are crucial for proper cell functions, remain poorly understood. The receptor tyrosine kinase MET phosphorylates IQGAP1 on Tyr1510. Separately, Src homology 2 (SH2) domains mediate protein–protein interactions by binding specific phosphotyrosine residues. Here, we investigate whether MET-catalyzed phosphorylation of Tyr1510 of IQGAP1 regulates the docking of SH2-containing proteins. Using a peptide array, we identified SH2 domains from several proteins, including the non-receptor tyrosine kinases Abl1 and Abl2, that bind to the Tyr1510 of IQGAP1 in a phosphorylation-dependent manner. Using pure proteins, we validated that full-length Abl1 and Abl2 bind directly to phosphorylated Tyr1510 of IQGAP1. In cells, MET inhibition decreases endogenous IQGAP1 phosphorylation and interaction with endogenous Abl1 and Abl2, indicating that binding is regulated by MET-catalyzed phosphorylation of IQGAP1. Functionally, IQGAP1 modulates basal and HGF-stimulated Abl signaling. Moreover, IQGAP1 binds directly to MET, inhibiting its activation and signaling. Collectively, our study demonstrates that IQGAP1 is a phosphotyrosine-regulated scaffold for SH2-containing proteins, thereby uncovering a previously unidentified mechanism by which IQGAP1 coordinates intracellular signaling.

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12

Ha, Byung Hak, Mark Adam Simpson, Anthony J. Koleske, and Titus J. Boggon. "Structure of the ABL2/ARG kinase in complex with dasatinib." Acta Crystallographica Section F Structural Biology Communications 71, no. 4 (March 20, 2015): 443–48. http://dx.doi.org/10.1107/s2053230x15004793.

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ABL2/ARG (ABL-related gene) belongs to the ABL (Abelson tyrosine-protein kinase) family of tyrosine kinases. ARG plays important roles in cell morphogenesis, motility, growth and survival, and many of these biological roles overlap with the cellular functions of the ABL kinase. Chronic myeloid leukemia (CML) is associated with constitutive ABL kinase activation resulting from fusion between parts of the breakpoint cluster region (BCR) andABL1genes. Similarly, fusion of theETV6(Tel) andARGgenes drives some forms of T-cell acute lymphoblastic leukemia (T-ALL) and acute myeloid leukemia (AML). Dasatinib is a tyrosine kinase inhibitor used for the treatment of CML by inhibiting ABL, and while it also inhibits ARG, there is currently no structure of ARG in complex with dasatinib. Here, the co-crystal structure of the mouse ARG catalytic domain with dasatinib at 2.5 Å resolution is reported. Dasatinib-bound ARG is found in the DFG-in conformation although it is nonphosphorylated on the activation-loop tyrosine. In this structure the glycine-rich P-loop is found in a relatively open conformation compared with other known ABL family–inhibitor complex structures.

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Duan, Daisy, Wanqing Lyu, Kuanlin Wu, Chunxiang Wu, Yong Xiong, and Anthony J. Koleske. "Abl2 mediates microtubule nucleation and repair via tubulin co-condensation." Biophysical Journal 122, no. 3 (February 2023): 124a. http://dx.doi.org/10.1016/j.bpj.2022.11.839.

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14

Sampson, Samuel, Trason Thode, Kevin Drenner, Ryan Rodriguez Del Villar, Annika Ozols, Mohan Kaadige, Alexis Weston, et al. "Abstract 1048: Synergistic drug combination of LSD1 and ABL2 inhibitors for Ewing's sarcoma identified in an arrayed CRISPR screen approach." Cancer Research 82, no. 12_Supplement (June 15, 2022): 1048. http://dx.doi.org/10.1158/1538-7445.am2022-1048.

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Abstract Background: Ewing's Sarcoma (ES) is a rare and aggressive pediatric bone tumor that is driven by a chromosomal translocation and fusion between EWS and FLI1 genes resulting in a chimeric protein. Nearly 85% of ES cases express the EWS/FLI protein which functions as a transcription factor and drives oncogenesis. EWS/FLI interacts with lysine-specific demethylase 1 (LSD1) that is highly expressed in pediatric sarcomas, to repress critical tumor suppressors. We have developed a potent reversible LSD1 inhibitor, SP-2577 (Seclidemstat), that shows the ability to impair tissue culture cell viability in multiple ES cell lines and is currently in clinical trials. A more favorable therapeutic response to SP-2577 may be obtained by combining drugs that target multiple pathways and/or inhibit resistance mechanisms. Experimental Design: In this study, we applied an arrayed CRISPR screening (Synthego) to identify survival genes that can be candidates for molecularly targeted drugs. Gene candidates were validated using western blot, qPCR, soft agar assay. Ewing’s Sarcoma A673 ABL2i knockdown and scramble cell lines were generated, implanted into nude mice, and treated with SP-2577. Lastly, combinational drug treatments using FDA-approved inhibitors with SP-2577 were tested in 2D and 3D cultures. Results: CRISPR druggable library screen identified that downregulation of several genes resulted in increased SP-2577 cytotoxicity in multiple ES cell lines. Importantly, ABL2 knockdown was found to have a significant synergy in combination with SP-2577 treatment, both in vitro and in vivo. siRNA knockdown of ABL2 in combination with SP-2577 treatment revealed an increase in JNK signaling and Cleaved Caspases-3 activation with decreased Src phosphorylation. This data suggests that downregulation of ABL2 in combination with SP-2577 treatment promotes activation of apoptosis pathways in ES. In addition, combination treatment of SP-2577 with drugs targeting ABL2 pathway showed high synergy in vitro. Conclusion: This study highlights the potential for a combination treatment of SP-2577 with ABL2 inhibitors in ES patients. Further, our observations support the capability of arrayed CRISPR screening to identify new therapeutic strategies in ES. Citation Format: Samuel Sampson, Trason Thode, Kevin Drenner, Ryan Rodriguez Del Villar, Annika Ozols, Mohan Kaadige, Alexis Weston, Serina Ng, Tithi Ghosh Halder, Shelby Rheinschmidt, David Anderson, Kevin Holden, Raffaella Soldi, Sunil Sharma. Synergistic drug combination of LSD1 and ABL2 inhibitors for Ewing's sarcoma identified in an arrayed CRISPR screen approach [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1048.

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Aras, Siddhesh, Hassan Arrabi, Neeraja Purandare, Maik Hüttemann, John Kamholz, Stephan Züchner, and Lawrence I. Grossman. "Abl2 kinase phosphorylates Bi-organellar regulator MNRR1 in mitochondria, stimulating respiration." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1864, no. 2 (February 2017): 440–48. http://dx.doi.org/10.1016/j.bbamcr.2016.11.029.

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Qiang, Xiao-Fei, Zheng-Wei Zhang, Qian Liu, Nan Sun, Liang-Liang Pan, Jing Shen, Tong Li, Chen Yun, Hui Li, and Li-Hua Shi. "miR-20a Promotes Prostate Cancer Invasion and Migration Through Targeting ABL2." Journal of Cellular Biochemistry 115, no. 7 (May 7, 2014): 1269–76. http://dx.doi.org/10.1002/jcb.24778.

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Malnassy, Gregory, Hao Wang, and Wei Qiu. "PPARγ is stabilized in response to alcohol in an ABL2-dependent manner." Alcohol 96 (November 2021): 103. http://dx.doi.org/10.1016/j.alcohol.2021.09.021.

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18

Gil-Henn, H., A. Patsialou, Y. Wang, M. S. Warren, J. S. Condeelis, and A. J. Koleske. "Arg/Abl2 promotes invasion and attenuates proliferation of breast cancer in vivo." Oncogene 32, no. 21 (July 9, 2012): 2622–30. http://dx.doi.org/10.1038/onc.2012.284.

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19

Xu, Bin, Can Wang, Ya‐Li Wang, Shu‐Qiu Chen, Jian‐Ping Wu, Wei‐Dong Zhu, Chun‐Ying Wang, et al. "miR‐143 inhibits renal cell carcinoma cells metastatic potential by suppressing ABL2." Kaohsiung Journal of Medical Sciences 36, no. 8 (March 20, 2020): 592–98. http://dx.doi.org/10.1002/kjm2.12207.

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Kazi, Julhash U., Kaja Rupar, Alissa Marhäll, Sausan A. Moharram, Fatima Khanum, Kinjal Shah, Mohiuddin Gazi, et al. "ABL2 suppresses FLT3-ITD-induced cell proliferation through negative regulation of AKT signaling." Oncotarget 8, no. 7 (January 10, 2017): 12194–202. http://dx.doi.org/10.18632/oncotarget.14577.

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Wu, Kuanlin, Hanzhi Wu, Wanqing Lyu, Youngjoo Kim, Cristina M. Furdui, Karen S. Anderson, and Anthony J. Koleske. "Platelet-derived growth factor receptor beta activates Abl2 via direct binding and phosphorylation." Journal of Biological Chemistry 297, no. 1 (July 2021): 100883. http://dx.doi.org/10.1016/j.jbc.2021.100883.

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Simpson, Mark A., William D. Bradley, David Harburger, Maddy Parsons, David A. Calderwood, and Anthony J. Koleske. "Direct Interactions with the Integrin β1 Cytoplasmic Tail Activate the Abl2/Arg Kinase." Journal of Biological Chemistry 290, no. 13 (February 18, 2015): 8360–72. http://dx.doi.org/10.1074/jbc.m115.638874.

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Jacobsen, Freja Aksel, Alexander N. Scherer, Jeppe Mouritsen, Hera Bragadóttir, B. Thomas Bäckström, Samra Sardar, Dan Holmberg, Anthony J. Koleske, and Åsa Andersson. "A Role for the Non-Receptor Tyrosine Kinase Abl2/Arg in Experimental Neuroinflammation." Journal of Neuroimmune Pharmacology 13, no. 2 (March 17, 2018): 265–76. http://dx.doi.org/10.1007/s11481-018-9783-8.

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Hoj, Jacob P., Benjamin Mayro, and Ann Marie Pendergast. "A TAZ-AXL-ABL2 Feed-Forward Signaling Axis Promotes Lung Adenocarcinoma Brain Metastasis." Cell Reports 29, no. 11 (December 2019): 3421–34. http://dx.doi.org/10.1016/j.celrep.2019.11.018.

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Liu, Gaohua, Yuanpeng J. Huang, Rong Xiao, Dongyan Wang, Thomas B. Acton, and Gaetano T. Montelione. "NMR structure of F-actin-binding domain of Arg/Abl2 from Homo sapiens." Proteins: Structure, Function, and Bioinformatics 78, no. 5 (November 24, 2009): 1326–30. http://dx.doi.org/10.1002/prot.22656.

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Amado-Azevedo, Joana, Anne-Marieke D. van Stalborch, Erik T. Valent, Kalim Nawaz, Jan van Bezu, Etto C. Eringa, Femke P. M. Hoevenaars, et al. "Depletion of Arg/Abl2 improves endothelial cell adhesion and prevents vascular leak during inflammation." Angiogenesis 24, no. 3 (March 26, 2021): 677–93. http://dx.doi.org/10.1007/s10456-021-09781-x.

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AbstractEndothelial barrier disruption and vascular leak importantly contribute to organ dysfunction and mortality during inflammatory conditions like sepsis and acute respiratory distress syndrome. We identified the kinase Arg/Abl2 as a mediator of endothelial barrier disruption, but the role of Arg in endothelial monolayer regulation and its relevance in vivo remain poorly understood. Here we show that depletion of Arg in endothelial cells results in the activation of both RhoA and Rac1, increased cell spreading and elongation, redistribution of integrin-dependent cell-matrix adhesions to the cell periphery, and improved adhesion to the extracellular matrix. We further show that Arg is activated in the endothelium during inflammation, both in murine lungs exposed to barrier-disruptive agents, and in pulmonary microvessels of septic patients. Importantly, Arg-depleted endothelial cells were less sensitive to barrier-disruptive agents. Despite the formation of F-actin stress fibers and myosin light chain phosphorylation, Arg depletion diminished adherens junction disruption and intercellular gap formation, by reducing the disassembly of cell-matrix adhesions and cell retraction. In vivo, genetic deletion of Arg diminished vascular leak in the skin and lungs, in the presence of a normal immune response. Together, our data indicate that Arg is a central and non-redundant regulator of endothelial barrier integrity, which contributes to cell retraction and gap formation by increasing the dynamics of adherens junctions and cell-matrix adhesions in a Rho GTPase-dependent fashion. Therapeutic inhibition of Arg may provide a suitable strategy for the treatment of a variety of clinical conditions characterized by vascular leak.

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Lin, Y. C., M. F. Yeckel, and A. J. Koleske. "Abl2/Arg Controls Dendritic Spine and Dendrite Arbor Stability via Distinct Cytoskeletal Control Pathways." Journal of Neuroscience 33, no. 5 (January 30, 2013): 1846–57. http://dx.doi.org/10.1523/jneurosci.4284-12.2013.

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MacGrath, Stacey M., and Anthony J. Koleske. "Arg/Abl2 Modulates the Affinity and Stoichiometry of Binding of Cortactin to F-Actin." Biochemistry 51, no. 33 (August 10, 2012): 6644–53. http://dx.doi.org/10.1021/bi300722t.

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Shaw, Juliana E., Michaela B. C. Kilander, Yu-Chih Lin, and Anthony J. Koleske. "Abl2:Cortactin Interactions Regulate Dendritic Spine Stability via Control of a Stable Filamentous Actin Pool." Journal of Neuroscience 41, no. 14 (February 23, 2021): 3068–81. http://dx.doi.org/10.1523/jneurosci.2472-20.2021.

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De Marco, S., B. Torsello, E. Minutiello, S. Bombelli, C. Grasselli, S. Eriani, N. Zucchini, et al. "TGF-β1, Lox and Arg/Abl2 interact to promote clear cell renal cell carcinoma progression." European Urology Open Science 20 (October 2020): S63. http://dx.doi.org/10.1016/s2666-1683(20)35397-0.

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Adegbesan, Sherifat Ibidunni, Samuel Olubodun Obasa, and Ikililu Abdulraheem. "Growth performance, haematology and histopathology of African catfish (Clarias gariepinus) fed varying levels of Aloe barbadensis leaves." Journal of Fisheries 6, no. 1 (February 1, 2018): 553–62. http://dx.doi.org/10.17017/j.fish.31.

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One hundred and twenty Clarias gariepinus fingerlings (2.33 ± 0.07 g) were fed with 40% crude protein diets containing three concentrations of Aloe barbadensis leaves-paste: ABL1, 1%; ABL2, 2%; ABL3, 3%, and control, 0% ad libitum twice daily for 12 weeks. Mean weight gain and percentage weight gain increased (P < 0.05) as concentration of A. barbadensis increased. Survival rate decreased as concentration of paste increased. Differences (P < 0.05) seen in packed cell volume (PCV), haemoglobin (Hb), and red blood cell (RBC), thus highest in ABL3: PCV (36.67 ± 0.89%), Hb (12.37 ± 0.37 g dl–1) and RBC (3.47 ± 0.08×106 L–1) and lowest in control: PCV (22.0 ± 0.58%), Hb (7.37 ± 0.20 g dl–1) and RBC (2.07 ± 0.06 ×106 L–1). Liver histology of control fish was normal, while fatty degenerations were seen in the treated fish. The histology of fish kidney was normal in all treatments. The study concluded that 1% A. barbadensis leaves-paste could effectively improve growth performance, nutrient utilization and survival of cultured C. gariepinus.

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Ibidunni, Adegbesan Sherifat, Obasa Samuel Olubodun, and Abdulraheem Ikililu. "Growth performance, haematology and histopathology of African catfish (Clarias gariepinus) fed varying levels of Aloe barbadensis leaves." Journal of Fisheries 6, no. 1 (February 1, 2018): 553. http://dx.doi.org/10.17017/jfish.v6i1.2018.245.

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One hundred and twenty Clarias gariepinus fingerlings (2.33 ± 0.07 g) were fed with 40% crude protein diets containing three concentrations of Aloe barbadensis leaves-paste: ABL1, 1%; ABL2, 2%; ABL3, 3%, and control, 0% ad libitum twice daily for 12 weeks. Mean weight gain and percentage weight gain increased (P < 0.05) as concentration of A. barbadensis increased. Survival rate decreased as concentration of paste increased. Differences (P < 0.05) seen in packed cell volume (PCV), haemoglobin (Hb), and red blood cell (RBC), thus highest in ABL3: PCV (36.67 ± 0.89%), Hb (12.37 ± 0.37 g dl–1) and RBC (3.47 ± 0.08×106 L–1) and lowest in control: PCV (22.0 ± 0.58%), Hb (7.37 ± 0.20 g dl–1) and RBC (2.07 ± 0.06 ×106 L–1). Liver histology of control fish was normal, while fatty degenerations were seen in the treated fish. The histology of fish kidney was normal in all treatments. The study concluded that 1% A. barbadensis leaves-paste could effectively improve growth performance, nutrient utilization and survival of cultured C. gariepinus.

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Courtemanche, Naomi, Stacey M. Gifford, Mark A. Simpson, Thomas D. Pollard, and Anthony J. Koleske. "Abl2/Abl-related Gene Stabilizes Actin Filaments, Stimulates Actin Branching by Actin-related Protein 2/3 Complex, and Promotes Actin Filament Severing by Cofilin." Journal of Biological Chemistry 290, no. 7 (December 24, 2014): 4038–46. http://dx.doi.org/10.1074/jbc.m114.608117.

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Salah, Eidarus, Emilie Ugochukwu, Alastair J. Barr, Frank von Delft, Stefan Knapp, and Jonathan M. Elkins. "Crystal Structures of ABL-Related Gene (ABL2) in Complex with Imatinib, Tozasertib (VX-680), and a Type I Inhibitor of the Triazole Carbothioamide Class." Journal of Medicinal Chemistry 54, no. 7 (April 14, 2011): 2359–67. http://dx.doi.org/10.1021/jm101506n.

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Zhong, Jinnan, Min Liu, Shi Chen, Shuang Liu, Fajiu Li, and Chenghong Li. "Study of the Regulatory Mechanism of miR-26a-5p in Allergic Asthma." Cells 12, no. 1 (December 22, 2022): 38. http://dx.doi.org/10.3390/cells12010038.

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Objective: Allergic asthma is a growing burden on national public health services due to its high prevalence. The aim of this experiment was to investigate whether miR-26a-5p affects cellular fibrosis and thus airway remodeling in asthmatic mice through the regulation of target genes. Methods: Screening for differentially expressed miRNAs in asthma model mice was carried out by constructing a mouse model of allergic asthma. qRT-PCR was performed to determine candidate miRNAs in each group of bronchial tissues. Western blot detection of the expression levels of predicted candidate target genes in each group of bronchial tissues was conducted. A dual luciferase assay was performed to validate the binding of miR-26a-5p to target genes. Fibronectin, a marker of cellular fibrosis, was detected via flow cytometry. CCK8 and BrdU staining were used to detect the proliferation ability of each group of cells. Results: miR-26a-5p is able to target and bind to ABL2 3′-UTR, MMP16 3′-UTR and PDE7A 3′-UTR sequences. After interference with miR-26a-5p, improved bronchial histopathology and reduced peribronchial collagen deposition were found. Compared with the model group, interference with miR-26a-5p reduced lung fibrosis, decreased fibroblasts and increased apoptosis in mouse bronchial tissues; overexpression of miR-26a-5p decreased apoptosis in mouse bronchial tissues. Compared with the model group, the serum levels of IL-4, IL-5, IL-13 and I IFN-γ were decreased in the miR-26a-5p inhibitor group and increased in the miR-26a-5p mimic group. The immunohistochemical results showed that the expression of ABL2, MMP16 and PDE7A was significantly reduced after intervention with miR-26a-5p. Compared with the model group, the apoptosis rate of cells in the miR-26a-5p inhibitor group of the allergic asthma model was upregulated, the levels of IL-4, IL-5, IL-13, IFN-γ and ROS were decreased, the expression of the miRNA and proteins of ABL2, MMP16 and PDE7A was decreased, the expression of LC3A and P62 was significantly increased and the expression of LC3B, Beclin1, Atg5 and fibrosis markers collagen I and α-SMA was decreased. Conclusion: miR-26a-5p affects cellular fibrosis and thus airway remodeling in asthmatic mice by regulating target genes.

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Nguyen, Lan T., Hazel Lum, Chinnaswamy Tiruppathì, and Asrar B. Malik. "Site-specific thrombin receptor antibodies inhibit Ca2+ signaling and increased endothelial permeability." American Journal of Physiology-Cell Physiology 273, no. 5 (November 1, 1997): C1756—C1763. http://dx.doi.org/10.1152/ajpcell.1997.273.5.c1756.

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Thrombin receptor is activated by thrombin-mediated cleavage of the receptor’s NH2 terminus between Arg-41 and Ser-42, generating a new NH2terminus that functions as a “tethered ligand” by binding to sites on the receptor. We prepared antibodies (Abs) directed against specific receptor domains to study the tethered ligand-receptor interactions required for signaling the increase in endothelial permeability to albumin. We used polyclonal Abs directed against the peptide sequences corresponding to the extracellular NH2 terminus [residues 70–99 (AbDD) and 1–160 (AbEE)] and extracellular loops 1 and 2 [residues 161–178 (AbL1) and 244–265 (AbL2)] of the seven-transmembrane thrombin receptor. Receptor activation was determined by measuring changes in cytosolic Ca2+ concentration ([Ca2+]i) in human dermal microvascular endothelial cells (HMEC) loaded with Ca2+-sensitive fura 2-acetoxymethyl ester dye. The transendothelial125I-labeled albumin clearance rate (a measure of endothelial permeability) was determined across the confluent HMEC monolayers. AbEE (300 μg/ml), directed against the entire extracellular NH2-terminal extension, inhibited the thrombin-induced increases in [Ca2+]iand the endothelial 125I-albumin clearance rate (>90% reduction in both responses). AbDD (300 μg/ml), directed against a sequence within the NH2-terminal extension, inhibited 70% of the thrombin-induced increase in [Ca2+]iand 60% of the increased125I-albumin clearance rate. AbL2 (300 μg/ml) inhibited these responses by 70 and 80%, respectively. However, AbL1 (300 μg/ml) had no effect on either response. We conclude that NH2-terminal extension and loop 2 are critical sites for thrombin receptor activation in endothelial cells and thus lead to increased [Ca2+]iand transendothelial permeability to albumin.

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Cong, X. L., B. Li, R. C. Yang, S. Z. Feng, S. J. Chen, and Z. C. Han. "Enhanced growth suppression of Philadephia1 leukemia cells by targeting bcr3/abl2 and VEGF through antisense strategy." Leukemia 19, no. 9 (July 21, 2005): 1517–24. http://dx.doi.org/10.1038/sj.leu.2403851.

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Shapiro, Lauren P., Mitchell H. Omar, Anthony J. Koleske, and Shannon L. Gourley. "Corticosteroid-induced dendrite loss and behavioral deficiencies can be blocked by activation of Abl2/Arg kinase." Molecular and Cellular Neuroscience 85 (December 2017): 226–34. http://dx.doi.org/10.1016/j.mcn.2017.10.007.

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39

Shimizu, Akio, Akiko Mammoto, Joseph E. Italiano, Elke Pravda, Andrew C. Dudley, Donald E. Ingber, and Michael Klagsbrun. "ABL2/ARG Tyrosine Kinase Mediates SEMA3F-induced RhoA Inactivation and Cytoskeleton Collapse in Human Glioma Cells." Journal of Biological Chemistry 283, no. 40 (July 25, 2008): 27230–38. http://dx.doi.org/10.1074/jbc.m804520200.

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40

Schwab, Claire, Amir Enshaei, Kathryn G. Roberts, Lisa J. Russell, Richard C. Harvey, I.-Ming L. Chen, Cheryl L. Willman, et al. "The Frequency and Outcome of Ph-like ALL Associated Abnormalities in Childhood Acute Lymphoblastic Leukaemia Treated on MRC UKALL2003." Blood 128, no. 22 (December 2, 2016): 2914. http://dx.doi.org/10.1182/blood.v128.22.2914.2914.

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Abstract Introduction: Incorporating cytogenetics into risk stratification for the treatment of childhood ALL has contributed to increased survival rates. However approximately 25% of patients, the B-other subgroup, harbour none of the known major chromosomal abnormalities. Within this group, Philadelphia-like (Ph-like) patients show a similar gene expression profile to those with the BCR-ABL1 fusion and share the same high risk of relapse. Ph-like ALL is genetically heterogeneous with some patients harbouring tyrosine kinase activating gene fusions, such as EBF1-PDGFRB, or activation of the JAK-STAT signalling pathway, making them amenable to targeted therapy with kinase inhibitors. Methods: We studied patients with B-other ALL entered to the MRC UKALL2003 treatment trial using a panel of break-apart FISH probes to identify rearrangements of PDGFRB/CSF1R , ABL1 , ABL2 and JAK2. Rearrangements of the CRLF2 gene were identified using break-apart FISH probes for CRLF2, P2RY8 and IGH and/or MLPA using the P335-ALL-IKZF1 kit (MRC Holland, The Netherlands). Where possible, partner genes were identified by cytogenetics and FISH. RNA samples from 135 of the B-other cohort were screened using a Taqman low density array (TLDA) to detect the Ph-like gene expression signature and P2RY8-CRLF2 gene fusion. The overlap between the two cohorts is shown in Figure 1. Results: Within this B-other cohort, rearrangement of CRLF2 was the most prevalent abnormality, occurring in 13% of patients (n=65/503), with two-thirds of them showing deletion of the PAR1 region, resulting in P2RY8-CRLF2 fusion (n=43) and the remaining third showing IGH-CRLF2 (n=22). Rearrangements of PDGFRB/CSF1R occurred in 3.4% of the cohort(n=17/491), while ABL1 (n=4/485), ABL2 (n=1/454) and JAK2 (n=2/481) rearrangements were rare, each occurring in less than 1% of B-other patients. Partner genes were identified in 17 cases with kinase rearrangements, with EBF1-PDGFRB being the most common (n=10). PAX5-JAK2 was identified in 2 patients and ATF7IP-PDGFRB, MEF2D-CSF1R, SSBP2-CSF1R, ETV6-ABL1 and ZC3HAV1-ABL2 in single cases. By TDLA, 33/135 (24%) patients tested positive for a Ph-like signature. In 9 patients the arrays indicated high expression of CRLF2 with 7 of them having a P2RY8-CRLF2 transcript by TLDA, which was confirmed by FISH in 5 cases and MLPA in another case. In the remaining patients, the mechanism of CRLF2 over-expression remains unknown as no P2RY8-CRLF2 transcript was detectedby TDLA and no material was available for FISH or MLPA. A single case negative for Ph-like signature tested positive for P2RY8-CRLF2 transcript. Seven patients showed an ABL-class rearrangement by cytogenetics and FISH (EBF1-PDGFRB, n=5; ETV6-ABL1, n=1; ABL1 rearrangement partner unknown, n=1). The genetics underlying the remaining cases is being further investigated by whole genome and transcriptome sequencing. Of the 102 patients negative for a Ph-like signature, 71 of them were tested by FISH for kinase fusions. In a single case positive for EBF1-PDGFRB by FISH, expression of the EBF1-PDGFRB transcript was confirmed by RT-PCR. The 5-year event free survival (EFS) of the entire B-other cohort was 82% with a relapse rate (RR) of 12%. Patients with rearrangements of PDGFRB/CSF1R (n=17)and those testing positive for a Ph-like expression signature (n=33) showed an inferior outcome, with EFS rates of 31% and 65% and RR of 64% and 28%, respectively (p<0.005). As we have previously demonstrated, patients with CRLF2 rearrangement showed a higher rate of relapse (23%), although it did not reach significance (p=0.129). Conclusion: This is the largest unbiased cohort of paediatric B-other ALL screened for ABL1, ABL2, PDGFRB/CSF1R and JAK2 fusions. We demonstrate that FISH can reliably detect the full spectrum of these genetic changes, most of which are cryptic by cytogenetic analysis. These abnormalities were mutually exclusive with an overall frequency in B-other ALL of ~15%. Patients with rearrangements of PDGFRB/CSF1R and those testing positive for a Ph-like gene expression had high rates of relapse. Given the efficacy of tyrosine kinase inhibitors in treatment of these patients, testing for these abnormalities should be integrated into future clinical trials. Disclosures Mullighan: Incyte: Membership on an entity's Board of Directors or advisory committees; Amgen: Speakers Bureau; Loxo Oncology: Research Funding.

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Ajibola, S. I., S. O. Obasa, A. K. Akintokun, and I. Abdulraheem. "Body weight changes, nutrient utilization and intestinal microflora of African catfish (Clarias gariepinus) fed Aloe barbadensis leaves." Nigerian Journal of Animal Production 43, no. 1 (January 27, 2021): 385–98. http://dx.doi.org/10.51791/njap.v43i1.2784.

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Immuno-nutrition studies have shown that some nutrients are linked to the immunological status of fish. Growth performance, nutrient utilization and intestinal microflora were examined in Clarias gariepinus. The 120 C. gariepimus fingerlings (weight, 2.33±0.07g)were fed Aloe barbadensis leaves-paste supplemented diets in 40L freshwater-filled plastic tanks ad libitum twice daily for 12 weeks. The experimental diets containing 40% crude protein were supplemented with three concentration of A. barbadensis leaves-paste: ABL1-1%; ABL2-2%; ABL3-3% and control-0%. Mean weight gain (MWG) and percentage weight gain (PWG) increased (p<0.05) as the concentration of A. barbadensis increased. MWG (17.95±0.78) and PWG (772.2±54.94) were highest in fish fed ABL3 and lowest MWG (11.92±1.16) and PWG (17.95±0.78) in fish fed control diet. Nutrients were better utilized among the diets supplemented group at different significant levels (p < 0.05). The highest value of ANPU was observed in ABL1 when compared to all other treatments including the control. Survival rate decreased as concentration of paste increased. There were no significant differences (p>0.05) in the total bacterial counts (TBC) in A. barbadensis leaves-paste supplemented diets and the control having the highest TBC (23.67 ±0.88 x 105 CFU/ml). Growth of total fungal counts (TFC) was not observed in ABLI. There was a reduction in TFC as the concentration increased in the other supplemented diets, and the control having the highest TFC (7.67 ± 0.44 x 105CFU/ml). The study concluded that inclusion of 1% A. barbadensis leaves-paste as supplement in the diet could effectively improve the growth performance, nutrient utilization and survival of cultured C. gariepinus. A. barbadensis leaves-paste could also reduce the microbial load of the fish.

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De Marco, S., B. Torsello, I. Morabito, S. Bombelli, C. Grasselli, N. Zucchini, G. Lucarelli, G. Strada, R. Perego, and C. Bianchi. "ABL2 kinase is involved in TGFB1-induced matrix degradation by invadopodia in clear cell renal cell carcinoma." European Urology Open Science 44 (October 2022): S142. http://dx.doi.org/10.1016/s2666-1683(22)01305-2.

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43

Torsello, Barbara, Sofia De Marco, Silvia Bombelli, Elisa Chisci, Valeria Cassina, Roberta Corti, Davide Bernasconi, Roberto Giovannoni, Cristina Bianchi, and Roberto A. Perego. "The 1ALCTL and 1BLCTL isoforms of Arg/Abl2 induce fibroblast activation and extra cellular matrix remodelling differently." Biology Open 8, no. 3 (March 5, 2019): bio038554. http://dx.doi.org/10.1242/bio.038554.

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44

Roberts, Kathryn G., Yongjin Li, Debbie Payne-Turner, Richard C. Harvey, Jinjun Cheng, Jinghui Zhang, Guangchun Song, et al. "Genomic Characterization and Experimental Modeling Of BCR-ABL1-Like Acute Lymphoblastic Leukemia." Blood 122, no. 21 (November 15, 2013): 232. http://dx.doi.org/10.1182/blood.v122.21.232.232.

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Abstract BCR-ABL1-like B-progenitor acute lymphoblastic leukemia (B-ALL) accounts for 10-15% of childhood B-ALL and is characterized by alteration of IKZFI, a gene expression profile similar to BCR-ABL1 ALL and poor outcome. Using next-generation sequencing, we have shown that BCR-ABL1-like ALL patients harbor genetic alterations activating kinase pathways that are sensitive to tyrosine kinase inhibitors (TKIs), and have shown that refractory BCR-ABL1-like ALL is responsive to TKIs in vivo (Weston et al., J. Clin. Oncol 2013). Furthermore, the outcome of ALL in adolescent and young adult (AYA) patients is inferior to children, yet the genetic basis underlying treatment failure is poorly understood. To define the frequency and genomic landscape of BCR-ABL1-like ALL in children, adolescents, and young adults we have extended our studies to include 665 high-risk childhood (<16 years, 14% BCR-ABL1-like), 370 adolescent (16-21 years, 21% BCR-ABL1-like) and 161 young adult (21-39 years; 26% BCR-ABL1-like) B-ALL cases from the Children's Oncology Group, St Jude Children's Research Hospital, Eastern Cooperative Oncology Group, MD Anderson Cancer Center and the Alliance - CALGB trials. Event-free survival (EFS) for BCR-ABL1-like cases was inferior to non BCR-ABL1-like cases with 5-year EFS rates of 40.0±7.1 vs 85.0±3.3 (p<0.0001) for adolescent cases and 16.1±8.5 vs 57.9±8.0 (p=0.006) for young adult cases. In each age group, 50-60% of BCR-ABL1-like cases harbored rearrangements of CRLF2 (IGH@-CRLF2 or P2RY8-CRLF2) (Fig. 1). To characterize the full spectrum of kinase lesions in the remaining BCR-ABL1-like ALL cases we performed mRNA-seq on pediatric (n=39), adolescent (n=21) and young adult (n=22) cases, and whole genome (WGS; n=18) or exome sequencing (n=10) on cases with matched tumor and normal material. Fusion transcripts were identified using deFuse and CICERO, a novel assembly-based structural variation detection method specifically designed for mRNA-seq analysis. We identified 23 different kinase rearrangements involving 7 tyrosine kinase or cytokine receptor genes. These consist of 5 ABL1, 2 PDGFRB, 8 JAK2 fusions and 2 EPOR translocations to IGH@ and IGK@ loci, along with new fusions involving the tyrosine kinases ABL2 (n=3), CSF1R (n=1), AKT2 (n=1) and STAT5B (n=1). We performed frequency testing for 15 of these fusions on 555 cases from the COG AALL0232 trial of high-risk B-ALL. Several alterations were recurrent in BCR-ABL1-like ALL, including NUP214-ABL1, RCSD1-ABL2, SSBP2-CSF1R, PAX5-JAK2 and EPOR translocations. Notably, we did not identify any of these fusions in non BCR-ABL1-like cases. The frequency of ABL1/ABL2 and EPOR translocations was consistent across all age groups (∼16% and 7% of BCR-ABL1-like cases, respectively), while JAK2 rearrangements were more common in young adult than in pediatric and adolescent ALL (12%). Importantly, ∼10% of BCR-ABL1-like ALL cases lacked a kinase-activating alteration on analysis of mRNA-seq data. Notably, we identified two additional cases with IL7R or SH2B3 sequence mutations, indicating the requirement for complementary approaches such as WGS to fully define the genomic landscape of BCR-ABL1-like ALL. Current functional studies include the development of experimental models using the Ba/F3 hematopoietic progenitor cell line, primary mouse pre-B cultures and the generation of xenografts to determine the role of these alterations in leukemogenesis, and to enable testing of targeted therapies. For example, we show that RCSD1-ABL1 and SSBP2-CSF1R confer factor-independent growth and constitutive activation of JAK/STAT pathways in Ba/F3 cells. Furthermore, RCSD1-ABL1 and SSBP2-CSF1R are both sensitive to the TKIs, imatinib (IC50 378nM and 327nM, respectively) and dasatinib (IC50 2.1nM and 2.5nM, respectively). Together, these complementary approaches will further define the genetic landscape of both pediatric and AYA ALL, and facilitate the development of diagnostic and therapeutic strategies to improve the treatment outcome for high-risk BCR-ABL1-like ALL patients. Disclosures: Hunger: Bristol Myers Squibb: Consultancy.

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Marchetti, Monia. "COVID-19-driven endothelial damage: complement, HIF-1, and ABL2 are potential pathways of damage and targets for cure." Annals of Hematology 99, no. 8 (June 24, 2020): 1701–7. http://dx.doi.org/10.1007/s00277-020-04138-8.

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Bordean, Maria-Evelina, Rodica Ana Ungur, Dan Alexandru Toc, Ileana Monica Borda, Georgiana Smaranda Marțiș, Carmen Rodica Pop, Miuța Filip, et al. "Antibacterial and Phytochemical Screening of Artemisia Species." Antioxidants 12, no. 3 (February 27, 2023): 596. http://dx.doi.org/10.3390/antiox12030596.

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Taking into account the increasing number of antibiotic-resistant bacteria, actual research focused on plant extracts is vital. The aim of our study was to investigate leaf and stem ethanolic extracts of Artemisia absinthium L. and Artemisia annua L. in order to explore their antioxidant and antibacterial activities. Total phenolic content (TPC) was evaluated spectrophotometrically. Antioxidant activity was evaluated by DPPH and ABTS. The antibacterial activity of wormwood extracts was assessed by minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) in Escherichia coli, Staphylococcus aureus, Listeria monocytogenes, and Salmonella enteritidis cultures, and by zone of inhibition in Klebsiella carbapenem-resistant enterobacteriaceae (CRE) and Escherichia coli extended-spectrum β-lactamases cultures (ESBL). The Artemisia annua L. leaf extract (AnL) exhibited the highest TPC (518.09 mg/mL) and the highest expression of sinapic acid (285.69 ± 0.002 µg/mL). Nevertheless, the highest antioxidant capacity (1360.51 ± 0.04 µM Trolox/g DW by ABTS and 735.77 ± 0.02 µM Trolox/g DW by DPPH) was found in Artemisia absinthium L. leaf from the second year of vegetation (AbL2). AnL extract exhibited the lowest MIC and MBC for all tested bacteria and the maximal zone of inhibition for Klebsiella CRE and Escherichia coli ESBL. Our study revealed that AbL2 exhibited the best antioxidant potential, while AnL extract had the strongest antibacterial effect.

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Tasian, Sarah K., Mignon L. Loh, and Stephen P. Hunger. "Philadelphia chromosome–like acute lymphoblastic leukemia." Blood 130, no. 19 (November 9, 2017): 2064–72. http://dx.doi.org/10.1182/blood-2017-06-743252.

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AbstractPhiladelphia chromosome (Ph)-like acute lymphoblastic leukemia (ALL), also referred to as BCR-ABL1–like ALL, is a high-risk subset with a gene expression profile that shares significant overlap with that of Ph-positive (Ph+) ALL and is suggestive of activated kinase signaling. Although Ph+ ALL is defined by BCR-ABL1 fusion, Ph-like ALL cases contain a variety of genomic alterations that activate kinase and cytokine receptor signaling. These alterations can be grouped into major subclasses that include ABL-class fusions involving ABL1, ABL2, CSF1R, and PDGFRB that phenocopy BCR-ABL1 and alterations of CRLF2, JAK2, and EPOR that activate JAK/STAT signaling. Additional genomic alterations in Ph-like ALL activate other kinases, including BLNK, DGKH, FGFR1, IL2RB, LYN, NTRK3, PDGFRA, PTK2B, TYK2, and the RAS signaling pathway. Recent studies have helped to define the genomic landscape of Ph-like ALL and how it varies across the age spectrum, associated clinical features and outcomes, and genetic risk factors. Preclinical studies and anecdotal reports show that targeted inhibitors of relevant signaling pathways are active in specific Ph-like ALL subsets, and precision medicine trials have been initiated for this high-risk ALL subset.

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Westermann, Jörg, Antje van Lessen, Claudia Schlimper, Gökben Baskaynak, Philipp Le Coutre, Bernd Dörken, and Antonio Pezzutto. "Simultaneous Cytokine Analysis by Cytometric Bead Array (CBA) Allows More Sensitive Detection of Leukemia-Reactive T Cells in Patients with Chronic Myeloid Leukemia." Blood 106, no. 11 (November 16, 2005): 2879. http://dx.doi.org/10.1182/blood.v106.11.2879.2879.

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Abstract T cells recognizing truly leukemia-specific antigens like bcr/abl or other leukemia-associated antigens such as proteinase-3 and WT-1 are present in the T cell repertoire of leukemia patients and several studies have suggested that anti-leukemic T cells might be of clinical relevance. Detection of these leukemia-reactive T cells in CML patients is generally hampered by their low frequency making in vitro prestimulation necessary in most cases. Furthermore, shaping of the T cell repertoire by deletion of high affinity leukemia-reactive T cells and functional unresponsiveness are likely to have additional influence on T cell detection in structural or functional assays. Aim of our study was the detection of T cells specific for different CML-associated antigens chronic phase CML patients, most of them under imatinib treatment. In peripheral blood of CML patients we used a novel T cell assay (cytometric bead array = CBA), g-interferon ELISpot and tetramer staining in order to detect CML-reactive T cells against several known and new epitopes from bcr3/abl2, proteinase-3, c-abl and SOCS-2. By the standard g-interferon ELISpot peptide-specific T cells were not detectable in the vast majority of patients (33/34). In contrast peptide-specific cytokine release was detected in some of the patients by CBA upon pulsing with peptides from bcr3/abl2, proteinase-3, c-abl and SOCS-2. Peptide-specific cytokine release was detected particulary against a HLA-B8-restricted peptide from the fusion region of bcr3/abl2 (3/9 cases), against a HLA-A2-restricted epitope from proteinase-3 (3/11 cases), against a HLA-A2-restricted peptide from SOCS-2 (4/11 cases) and against two HLA-A2 and -B8-restricted epitopes from c-abl (3/11 and 2/9 cases respectively). T cell reactivity against the HLA-class-I epitopes from c-abl and SOCS-2 is described here for the first time. Interestingly, peptide-specific cytokine release was predominantly TNF-a, a significant IFN-g secretion was detected only in a few cases raising questions about the responding cells and their functional status. By tetramer staining low frequency T cells recognizing the bcr3/abl2 fusion protein were detected only in 2/15 patients, but after prestimulation of PBMC bcr/abl-specific T cells could be detected in 4/8 HLA-B8+ patients. Low T cell frequeny and deletion of high avidity T cells is a general obstacle for immune monitoring in cancer patients which may explain negative results obtained by g-IFN-ELISpot or tetramer staining. Furthermore, in CML an altered cytokine secretion pattern of T cells might be an additional limitation of functional T cell assays. Summarizing, we have found T cells recognizing CML-associated antigens which display a TNF-a-dominated cytokine secretion profile. This would have been missed using a standard g-IFN-ELISpot assay both because of the cytokine pattern of the T cells and the sensitivity of the assay. Using CBA there is a higher chance to detect low frequency leukemia-reactive T cells and to identify new immunotherapeutic targets in CML.

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Ajibola, S. I., S. O. Obasa, A. K. Akintokun, and I. Abdulraheem. "Body weight changes, nutrient utilization and intestinal microflora of African catfish (Clarias gariepinus) fed Aloe barbadensis leaves." Nigerian Journal of Animal Production 43, no. 2 (January 9, 2021): 385–98. http://dx.doi.org/10.51791/njap.v43i2.725.

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Immuno-nutrition studies have shown that some nutrients are linked to the immunological status of fish. Growth performance, nutrient utilization and intestinal microflora were examined in Clarias gariepinus. The 120 C. gariepinus fingerlings (weight, 2.33±0.07g) were fed with Aloe barbadensis leaves-paste supplemented diets in 40L freshwater-filled plastic tanks ad libitum twice daily for 12 weeks. The experimental diets containing 40% crude protein were supplemented with three concentration of A. barbadensis leaves-paste: ABL1–1%; ABL2–2%; ABL3–3% and control–0%. Mean weight gain (MWG) and percentage weight gain (PWG) increased (p<0.05) as the concentration of A. barbadensis increased. MWG (17.95±0.78) and PWG (772.2±54.94) were highest in fish fed ABL3 and lowest MWG (11.92±1.16) and PWG (17.95±0.78) in fish fed control diet. Nutrients were better utilized among the diets supplemented group at different significant levels (p < 0.05). The highest value of ANPU was observed in ABL1 when compared to all other treatments including the control. Survival rate decreased as concentration of paste increased. There were no significant differences (p>0.05) in the total bacterial counts (TBC) in A. barbadensis leaves-paste supplemented diets and the control having the highest TBC (23.67 ± 0.88 x 105CFU/ml). Growth of total fungal counts (TFC) was not observed in ABL1. There was a reduction in TFC as the concentration increased in the other supplemented diets, and the control having the highest TFC (7.67 ± 0.44 x 105 CFU/ml). The study concluded that inclusion of 1% A. barbadensis leaves-paste as supplement in the diet could effectively improve the growth performance, nutrient utilization and survival of cultured C. gariepinus. A. barbadensis leaves-paste could also reduce the microbial load of the fish.

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Decool, Gauthier, Carine Domenech, Nathalie Grardel, Adriana Plesa, Imelda Raczkiewicz, Benoit Ducourneau, Philippe Ruminy, et al. "Efficacy of Tyrosine Kinase Inhibitor Therapy in a Chemotherapy-refractory B-cell Precursor Acute Lymphoblastic Leukemia With ZC3HAV1-ABL2 Fusion." HemaSphere 3, no. 3 (June 2019): e193. http://dx.doi.org/10.1097/hs9.0000000000000193.

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