Relevant bibliographies by topics / Abl2

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Academic literature on the topic 'Abl2'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Abl2"

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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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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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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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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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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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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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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Dissertations / Theses on the topic "Abl2"

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Yang, Yi. "Signal transduction of abscisic acid in Arabidopsis thaliana identification and characterisation of protein interaction partners of ABl2 /." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969393997.

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DE, MARCO SOFIA. "STUDY OF THE INTERACTIONS AMONG ARG/ABL2, TGF-β1 AND LOX IN CLEAR CELL RENAL CELL CARCINOMA PROGRESSION." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/263399.

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In circa il 25-30% dei pazienti con carcinoma renale a cellule chiare (ccRCC) la diagnosi viene fatta quando la malattia è già ad uno stadio avanzato e circa il 30% di questi pazienti presenta metastasi ossee. È stato descritto un coinvolgimento del TGF-β1 nel promuovere aggressività, invasione e metastasi ossee nel ccRCC. Noi abbiamo già dimostrato che l'enzima della matrice extracellulare lisil ossidasi (Lox), noto per promuovere la migrazione e l'invasione cellulare attraverso il riarrangiamento del citoscheletro, è overespresso nel ccRCC. Lox, attraverso l'attivazione degli osteoclasti e l'inibizione degli osteoblasti, ha un ruolo chiave nella formazione delle lesioni ossee premetastatiche nel carcinoma mammario e del colon. Noi abbiamo precedentemente evidenziato che la produzione di TGF-β1 è modulata dalla tirosina chinasi Arg nelle cellule tubulari renali umane. Arg modula, attraverso il riarrangiamento del citoscheletro, l'invasione e la metastatizzazione del carcinoma mammario e prostatico. In base a questi dati e utilizzando come modelli in vitro colture cellulari primarie e linee cellulari, abbiamo valutato le interazioni molecolari tra TGF-β1, Lox e Arg in cellule di ccRCC e gli effetti funzionali di queste interazioni sull'invasione tumorale e sul comportamento degli osteoclasti e degli osteoblasti responsabili della formazione di lesioni ossee premetastatiche. L'espressione e la secrezione di TGF-β1 e Lox, e l'espressione della proteina Arg erano aumentate nelle colture primarie di ccRCC rispetto a quelle di cortex normale. Nelle colture di ccRCC la secrezione di TGF-β1 e Lox era positivamente correlata. Il trattamento con TGF-β1 della linea cellulare di ccRCC, 786-O, aumentava l'espressione e la secrezione di Lox e riduceva il livello della proteina Arg. L'inibitore del recettore del TGF-β SB431542 contrastava questi effetti. L'inibizione del signaling Smad-dipendente del TGF-β con SIS3 e dell'attività del proteasoma con MG132 riaumentava il livello della proteina Arg. Il silenziamento di Arg con un siRNA specifico induceva nelle cellule 786-O un aumento della secrezione di TGF-β1 e Lox, contrastata dal trattamento con SB431542. Inoltre, il silenziamento di Arg nelle cellule 786-O ha ridotto l'invasione cellulare valutata con saggio di invasione 3D in collagene, anche in presenza del trattamento con TGF-β1. L'inibizione del signaling di TGF-β1 con SB431542 riduceva l'invasione cellulare anche in cellule silenziate per Arg. Il trattamento con terreni condizionati di cellule 786-O inibiva la proliferazione degli osteoblasti MC3T3-E1 e aumentava la differenziazione osteoclastica delle cellule RAW264.7, come valutato dalla colorazione della fosfatasi acida resistente al tartrato (TRAP). L'inibitore di Lox, βAPN, contrastava parzialmente questi effetti. I risultati preliminari ottenuti utilizzando i terreni condizionati di colture primarie di ccRCC hanno confermato queste osservazioni. Nel complesso questi dati suggeriscono che nelle cellule di ccRCC Arg modula la produzione di Lox mediante secrezione di TGF-β1 che, a sua volta, modula la stabilità della proteina Arg attraverso un pathway Smad-dipendente. La caratterizzazione delle complesse interazioni tra TGF-β1, Lox e Arg che modulano l'invasione delle cellule di ccRCC e il comportamento degli osteoblasti e degli osteoclasti coinvolti nella formazione di lesioni ossee premetastatiche, può far luce sui meccanismi molecolari della progressione del ccRCC.
About 25-30% of clear cell Renal Cell Carcinoma (ccRCC) patients show an advanced stage of disease at the time of diagnosis, and about 30% of these patients have matastasis affecting bones. An involvement of TGF-β1 in promoting ccRCC aggressiveness, invasion and bone metastasis has been described. We previously showed that the extracellular matrix modifying enzyme lysyl oxidase (Lox), which promotes cell migration and invasion through cytoskeleton rearrangement, was overexpressed in ccRCC. Lox has a key role in formation of premetastatic bone lesions in breast and colon cancer through osteoclast activation and osteoblast inhibition. Previous data evidenced that TGF-β1 production is modulated by Arg tyrosine kinase in human renal tubular cells. Arg modulates, through cytoskeleton rearrangement, invasion and metastasis of breast and prostate cancers. Based on these data and using in vitro models of primary cell cultures and cell lines, we evaluated the molecular interactions among TGF-β1, Lox and Arg in ccRCC cells and the functional effects of these interactions on tumor invasion and osteoclast and osteoblast behavior responsible for premetastatic bone lesion formation. The expression and secretion of TGF-β1 and Lox, and Arg protein expression, were increased in ccRCC versus normal cortex primary cultures. In ccRCC cultures TGF-β1 and Lox secretion were positively correlated. TGF-β1 treatment of ccRCC 786-O cell line upregulated Lox expression and secretion and downregulated Arg protein level. The TGFβ-receptor inhibitor SB431542 reverted these effects. Inhibition of Smad-dependent TGF-β pathway by SIS3 and proteasome activity by MG132 rescued Arg protein level. Arg silencing by siRNA in 786-O cells induced an increment of TGF-β1 and Lox secretion, reverted by SB431542 treatment. Moreover, Arg silencing in 786-O cells decreased cell invasion analyzed by 3D invasion assay in collagen, even in presence of TGF-β1 treatment. TGF-β1 signalling inhibition with SB431542 reduced cell invasion even in Arg silenced cells. Treatment with 786-O conditioned media inhibited MC3T3-E1 osteoblast proliferation and increased osteoclastic differentiation of RAW264.7 cells, as evaluated by TRAP staining. Lox inhibitor βAPN partially reverted these effects. Preliminary results obtained using conditioned media of ccRCC primary cultures confirmed these observations. Overall, these data suggest that in ccRCC cells Arg modulates Lox production by secretion of TGF-β1 that, in turn, modulates Arg protein stability through a Smad-dependent pathway. The characterization of the complex interactions among TGF-β1, Lox and Arg, which modulate ccRCC cell invasion and osteoblast and osteoclast behavior involved in premetastatic bone lesion formation, can shed light on the molecular mechanisms of ccRCC progression.
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ANGELONI, VALENTINA. "Studio e caratterizzazione delle isoforme della tirosino chinasi non recettoriale ARG nel differenziamento neuronale in vitro." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2010. http://hdl.handle.net/10281/7823.

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Il gene umano ARG (o ABL2) codifica per una proteina che appartiene alla sottofamiglia Abelson delle tirosino chinasi non recettoriali (Kruh et al.,1990; Perego et al., 1991). Arg in vitrù dei domini di legame alle proteine del citoscheltro (Hernandez et al., 2004a e Miller et al., 2004) e al coinvolgimento, mediante la sua attività chinasica, nei pathway molecolari di riarrangiamento del citoscheletro (Galkin et al., 2005) è attivamente coinvolto nel processo di neuritogenesi e di formazione e funzione delle sinapsi (Koleske et al., 1998). Come per c-Abl anche per Arg sono state descritte, per splicing alternativo dell’esone 1, due isoforme N-terminali (1A e 1B) (Kruh et al., 1990). Nel nostro laboratorio sono state identificate con metodiche di RT-PCR qualitativa nuovi trascritti di Arg che predicono isoforme con diverse estremità 5' e 3' (Perego et al., 2005). Per quanto riguarda le estremità 5' si è dimostrato che l’escissione alternativa dell’esone 2, giustapposto all’esone 1A o 1B, produce quattro diversi trascritti definiti B-Long (BL), B-Short (BS), A-Long (AL) e A-Short (AS) (Perego et al., 2005). Le forme "Long" mantengono l’esone 2 costituito da 63 paia di basi e lo splicing alternativo di questo esone non interrompe l’open reading frame della proteina. All’estremità 3' sono state invece identificate 2 ulteriori isoforme che differiscono per una sequenza, detta ΔCT, di 309 paia di basi corrispondenti a 103 amminoacidi e che sono state definite come "Short" e "Long" (CTS e CTL) a seconda che abbiano perso o meno questa sequenza; la delezione della sequenza ΔCT elimina parte del primo sito legante l’actina (Perego et al., 2005). I trascritti corrispondenti alle diverse estremità 5' e 3' sono differentemente espressi nei vari tipi cellulari e durante la differenziazione mieloide e linfoide (Perego et al., 2005). Combinando i diversi splicing dell’estremità 5' e 3' è possibilie ipotizzare l’esistenza di otto diverse isoforme full-length di Arg (ASCTS, ALCTS, ASCTL, ALCTL, BSCTS, BLCTS, BSCTL e BLCTL), dotate di diversa possibilità di interazione con il citoscheletro e differente coinvolgimento in pathways metabolici. Per dimostrare l’effettiva espressione endogena dei trascritti corrispondenti alle otto diverse isoforrme full-ength di Arg abbiamo prima analizzato, mediante Real-Time PCR, il pattern d’espressione delle diverse estremità 5' e 3' del trascritto di Arg nelle linee cellulari renali Hek 293T e Caki-1. Abbiamo così evidenziato che le estremità 5' sono tutte espresse solo nelle cellule Caki-1, a differenza delle cellule Hek 293T, che esprimono solo le forme B. Le estremità 3' invece sono espresse, anche se con rapporti quantitativi differenti, in entrambe le linee. La linea cellulare Caki-1 è stata quindi utilizzata per dimostrare l’effettiva espressione dei trascritti corrispondenti alle 8 diverse isoforme di Arg mediante cicli sequenziali di PCR (Long e Nested PCR) che utilizzavano combinazioni di diversi primers specifici. La presenza di amplificati della dimensione attesa per le diverse isoforme full-length dimostra, in queste linea cellulare, l’effettiva espressione di tutti 8 i trascritti full-length di Arg predetti. Una volta dimostrata l’esistenza delle otto isoforme di Arg abbiamo cercato di valutarne il coinvolgimento in un modello di differenziamento neuronale "in vitro", basandoci sui dati di letteratura che vedono Arg coinvolto nella neuritogenesi e nella formazione e funzione delle sinapsi (Koleske et al., 1998). Pertanto la linea cellulare di neuroblastoma umano SH-SY5Y è stata indotta al differenziamento per trattamento con ATRA (All-Trans-Retinoic-Acid) e Abeta (peptide amiloidogeno (Aβ1-42)), che come documentato in letteratura è dotata a basse concentrazioni di attività neurotrofica (Susen and Blochl, 2005). L’effetto differenziativo prodotto sulla linea cellulare SH-SY5Y da questi trattamenti è stato documentato mediante analisi morfologica e in immunofluorescenza, mentre tramite Real-Time PCR e western blot si sono quantificati i livelli del trascritto e della proteina di Arg prima e dopo trattamento ed analizzati i livelli di espressione relativa dei trascritti corrispondenti alle diverse estremità 5' e 3', allo scopo di evidenziare eventuali variazioni in corso di differenziamento. Inoltre sulla base dei dati di letteratura che evidenziano il ruolo di Arg come promotore della neuritogenesi in cellule di neuroblastoma N2A (Hernandez et al., 2004b) per attivazione dell’inibitore di Rho p190RhoGAP, in seguito a fosforilazione Arg-dipendente della sua tirosina 1105 (Y1105), è stato analizzato il livello di p190RhoGAP fosforilato in Y1105. Nelle cellule SH-SY5Y, trattate con 20μM ATRA per 6 giorni, Arg sembra essere coinvolto in un pathway neurodifferenziativo p190RhoGAP-dipendente, infatti il trascritto totale di Arg incrementa e sebbene il livello proteico di Arg sia paragonabile a quello delle cellule controllo, il livello di p190RhoGAP fosforilato in Y1105 risulta aumentato. Arg sembra essere coinvolto anche nel processo neurodifferenziativo a cui le cellule SH-SY5Y vanno incontro per trattamento con 0,01μM Abeta per 72 ore, infatti l’analisi mediante Real-Time PCR e western blot ha mostrato un’over-espressione sia del trascritto che della proteina totale di Arg nelle cellule SH-SY5Y trattate con Abeta rispetto alle cellule controllo. Inoltre il pattern di espressione delle isoforme di Arg, analizzato tramite Real-Time PCR, ha mostrato una maggiore espressione del trascritto con estremità 3' di tipo CTL rispetto alla controparte CTS, al contrario di quanto succede nelle cellule controllo. L’analisi del livello di p190RhoGAP fosforilato in tirosina 1105 non mostra però nelle cellule trattate con Abeta una variazione rispetto alle cellule controllo. Questi dati fanno ipotizzare un coinvolgimento di Arg in un pathway di neuritogenesi p190RhoGAP-indipendente, diverso quindi da quello attivato dal trattamento con ATRA nelle cellule SH-SY5Y. Del resto è stato anche descritto che in cellule di neuroblastoma N2A la transfezione di Arg può indurre la neuritogenesi senza indurre inibizione di Rho e quindi attraverso un pathway p190RhoGAP-indipendente (Hernandez et al., 2004b). Ulteriori studi sono in corso per valutare il coinvolgimento di Arg in pathway alternativi a quello di Rho nel processo di neuritogenesi indotto da Abeta. Date le sopra citate caratteristiche di Arg e il suo ruolo nel sistema nervoso centrale visto il ruolo di Abl nel taglio proteolitico del precursore della proteina amiloide (APP) (Perkinton et al., 2004) Abbiamo valutato l’espressione di Arg e delle sue isoforme anche in colture primarie di fibroblasti prelevati da pazienti affetti da Alzheimer rispetto ai controlli sani, riscontrando un’over-espressione del trascritto totale di Arg. Questo dato rappresenta il punto di partenza per studi fututri che mirino a definire il possibile coinvolgimento di Arg nel metabolismo della proteina precursore dall’amiloide APP. Ulteriori studi verranno eseguiti utilizzando concentrazioni potenzialmente neurotossiche di Abeta (2,5μM) per stimolare le cellule SH-SY5Y al fine di valutarne l’effetto sull’espressione delle isoforme di Arg e sulla morfologia cellulare. Per valutare se le otto diverse isoforme full-length di Arg possono avere ruoli diversi nel differenziamento neuronale abbiamo anche approntato studi di tipo funzionale. Transfettando nella linea cellulare SH-SY5Y le otto diverse isoforme di Arg clonate nel vettore di espressione pFlagCMV2. Questi esperimenti hanno evidenziato che le isoforme BLCTL e BSCTL inducono nelle cellule transfettate l’acquisizione di una morfologia più rotondeggiante e una significativa diminuzione dello "spreading cellulare" rispetto alle cellule transfettate con il vettore controllo (LAC Z). L’isoforma BLCTS è invece tra le isoforme B quella che induce una maggiore produzione di protrusioni cellulari quando transfettate nella linea SH-SY5Y. In seguito a transfezione con le isoforme A, normalmente non espresse in questo tipo cellulare, ed in particolare con l’isoforma ALCTS, le cellule sviluppano un fenotipo ricco di estroflessioni di diversa lunghezza e spesso filopodiformi. Dato il ruolo di Arg, documentato in letteratura, nel riarrangiamento del citoscheletro (Galkin et al., 2005), abbiamo voluto poi valutare l’effetto sul citoscheletro di actina e tubulina dell’over-espressione delle isoforme BLCTS e ALCTS, che quando over-espresse inducono in modo più evidente la formazione di estroflessioni cellulari. Dall’analisi in immunofluorescenza delle cellule transfettate con le due isoforme BLCTS e ALCTS è emerso che quando nelle cellule SH-SY5Y viene over-espressa l’isoforma BLCTS la distribuzione dell’F-actina e della tubulina è corticale e paragonabile a quella delle cellule non transfettate mentre nelle cellule che over-esprimono l’isoforma ALCTS l’F-actina ha ancora una distribuzione corticale e paragonabile a quella delle cellule non transfettate, mentre la tubulina si accumula nel citoplasma dove colocalizza con Arg, diffondendo anche nel nucleo. Verranno eseguiti ulteriori studi per approfondire l’effetto dell’over-espressione delle singole isoforme, sia tramite trasfezioni stabili che inducibili delle otto isoforme full-length di Arg.
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Lee, Jennifer Kim. "A Novel Role for Abelson Tyrosine-Protein Kinase 2| Characterization of Abl2 in Regulating Myoblast Proliferation and Muscle Fiber Length." Thesis, New York University, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10258043.

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Skeletal muscle generates contractile forces that allow the body to execute movements for walking, speaking and breathing. Although we understand a great deal about the steps of muscle formation, the mechanisms that control muscle size are poorly understood. Even less is known about how muscles interact with skeletal elements, including connective tissue, tendon and bone. This dissertation describes a novel role for Abelson tyrosine-protein kinase 2, a non-receptor tyrosine kinase, during muscle development. First, I characterize the defects in skeletal muscle of abl2 mutant mice and show that muscle fibers in the diaphragm and other muscles are extraordinarily long in abl2 mutant mice. As a consequence of expansion of the diaphragm muscle, the central tendon of the diaphragm is proportionally reduced in size. Second, I demonstrate that abl2 controls muscle size by regulating myoblast proliferation. Third, I show that Abl2 acts in myoblasts to attenuate their proliferation, thereby limiting myoblast fusion and muscle fiber size. Fourth, I show that the exercise endurance of abl2 mutant mice is diminished, likely due to the compensatory reduction in size of the diaphragm central tendon. Finally, I provide evidence for signaling between muscle cells and tendon cells that induces tendon cell differentiation.

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Thai, Minh. "RIN1 activates ABL oncoproteins and its required for full BCR-ABL1 mediated transformation." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1790313631&sid=11&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Dasgupta, Yashodhara. "NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/239008.

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Biology
Ph.D.
BCR-ABL1 results from t(9;22)(q34;q11) reciprocal translocation resulting in BCR-ABL1 kinase expression, initiating chronic myeloid leukemia in chronic phase (CML-CP). At the initial stages of CML-CP both oncogenic BCR-ABL1 kinase and normal ABL1 kinase are expressed, however, loss of ABL1 kinase expression in CML-CP can result from an interstitial deletion in the normal chromosome 9 [del(9q34)] which may be combined with the transcriptional silencing of the alternative ABL1 promoter within the translocation eventually leading to disease progression and drug resistance. We found that BCR-ABL1 Abl1-/- cells generated a CML-blast phase (BP)-like disease phenotype in NOD-SCID mice compared to the BCR-ABL1 Abl1+/+ cells. To determine the mechanisms responsible for blastic transformation of BCR-ABL1 Abl1-/- cells, we examined the role of ABL1 in proliferation, differentiation, apoptosis, genomic instability, and stemness. The presence of ABL1 inhibited proliferation in BCR-ABL1 cells as BCR-ABL1 Abl1-/- cells had higher clonogenic activity and proliferative rate compared to their wild-type counterparts. ABL1 is essential for myeloid differentiation since BCR-ABL1 Abl1-/- cells showed an immature blast phenotype when stained with Wright-Giemsa and myeloid differentiation markers Gr-1 and CD11b. ABL1 promoted apoptosis in response to genotoxic stress as revealed by reduced clonogenicity and expression of p53, phosphoserine-15 p53 and activated caspase 3 in BCR-ABL1 Abl1+/+ compared to knock-out cells. Although the absence of ABL1 did not enhance ROS and oxidative DNA damage, it appears that an impaired DNA damage response may be responsible for higher chromosome numbers and an accumulation of high numbers of chromosomal aberrations in BCR-ABL1 Abl1-/- cells. We detected an expansion of Lin-c-Kit+Sca-1+ leukemia stem cells (LSCs) in BCR-ABL1 Abl1-/- cells compared to BCR-ABL1 Abl1+/+ or non-transformed counterparts; among the LSCs, there was a higher percentage of CD34-Flt3- long-term and CD34+Flt3- short-term stem cells. These results showed that ABL1 is involved in regulating the LSC compartment in BCR-ABL1 cells. DNA microarray analysis revealed changes in mRNA levels of several genes involved in proliferation, myeloid differentiation, apoptosis, DNA damage response and `stemness' in BCR-ABL1 Abl1-/- cells in comparison to BCR-ABL1 Abl1+/+ cells. Together, these results demonstrate a critical role of ABL1 as a tumor suppressor in BCR-ABL1-induced leukemia, prolonging survival in mice by suppressing proliferation and expansion of LSC, inducing myeloid differentiation, apoptosis and DNA damage response in BCR-ABL1 cells. Loss of ABL1 was also found to contribute to Imatinib resistance in BCR-ABL1 cells. Moreover, we hypothesized that enhancement of the tumor-suppressor function of ABL1 may have a significant impact on CML treatment. A small molecule activator of ABL1 kinase, 5-(1,3-diaryl-1H-pyrazol-4-yl)hydantoin (DPH), have been reported to interact with the myristoyl-binding site of ABL1 and destabilize the bent conformation of the á1 helix, thereby preventing the auto-inhibitory conformation. Western blot analysis revealed partially restored activation of ABL1 kinase when Imatinib-treated cells were incubated with DPH. DPH along with Imatinib was found to inhibit viability of BCR-ABL1 Abl1+/+ cells but not BCR-ABL1 Abl1-/- cells demonstrating its ABL1-specific mode of action. DPH when used in combination with tyrosine kinase inhibitors such as Imatinib and Ponatinib inhibited growth of CML CD34+ cells, Philadelphia chromosome-positive B-Acute Lymphoblastic Leukemia (Ph+B-ALL) cells and relapsed Ph+B-ALL cells harboring T315I mutation without affecting normal counterparts. A similar inhibitory effect was observed when TEL-ABL1-expressing cell lines and NUP214-ABL1-expressing murine bone marrow cells were treated with DPH and Imatinib, as well as Acute Myeloid Leukemia (AML) cells expressing FLT3-ITD mutation when treated with DPH in combination with AC220 which is the FLT3-ITD inhibitor. In summary, ABL1 is a potential tumor-suppressor in BCR-ABL1-induced leukemia and stimulation of its function may play a significant role in the development of novel therapeutic strategies for CML and other Fusion Tyrosine Kinase (FTK)-mediated hematologic malignancies.
Temple University--Theses
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Maletzke, Saskia [Verfasser], Steffen [Akademischer Betreuer] Koschmieder, and Burkhard [Akademischer Betreuer] Gess. "Die duale Hemmung der BCR-ABL1 Kinase und des Proteasoms als neuer Therapieansatz in der BCR-ABL positiven akuten lymphatischen Leukämie / Saskia Maletzke ; Steffen Koschmieder, Burkhard Gess." Aachen : Universitätsbibliothek der RWTH Aachen, 2021. http://d-nb.info/1229991301/34.

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Berglind, Johan, and Markus Hansson. "Låneförbudet i ABL." Thesis, Örebro University, Department of Behavioural, Social and Legal Sciences, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-554.

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I den här uppsatsen har vi undersökt och behandlat låneförbudet som återfinns i ABL 12:7 och i kap 21 i nya ABL. Vi har undersökt om lagen uppfyller sina syften samt vilka syften som lagstiftaren har haft. Intressant är att en ny ABL träder i kraft den 1 januari 2006. Vi har utgått från lagstiftningen och sedan följt upp med rättspraxis och doktrin.

Under arbetets gång upptäckte vi luckor i lagstiftningen vilket medför att syftena bakom lagstiftningen inte kom till sin fulla rätt. Luckorna öppnar möjligheter att kringgå låneförbudet med tämligen enkla metoder. Vi har bland annat undersökt kringgående av lagstiftningen med hjälp utav efterföljande finansiering samt ett kringgående med hjälp av andra rättsobjekt.

Med efterföljande finansiering menas att ett bolag köps med bolagets egna pengar, med hjälp av undantaget för koncernlån. Ett kringgående med hjälp utav andra rättsobjekt kan se ut på lite olika sätt. I vårt arbete har vi använt av oss utav en fysisk person samt ett handelsbolag. Ett kringgående av lagstiftningen möjliggörs genom att andra rättsobjekt än aktiebolag ej lyder under aktiebolagslagen i stora drag.

Dessa handlingar rör sig inom ett grått område inom juridiken och gör låneförbudet till ett tämligen trubbigt redskap.

Eftersom låneförbudet tillhör specialstraffrätten möjliggörs kringgående av lagstiftningen då restriktiv lagtolkning måste användas. Faller en handling inte in ordagrant i vad som står i lagtexten är kringgåendet av låneförbudet både i nya och gamla ABL ett faktum.

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Peters, Elaine. "Holistic Evaluation of Peer Writings by Able and Less Able Readers in Eighth and Tenth Grades." Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc331667/.

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The purpose of this study was to examine the use of general impression scoring by teachers and students, and to compare the criteria used in evaluating student writings. Subjects for the study were 40 eighth grade and tenth grade students of varying reading ability in regular English classes in a suburban school district. Teachers and students evaluated two sets of writings in the narrative, classificatory and descriptive modes, generated by ninth grade students in regular English classes in the same school district. In addition, a comment, citing criteria upon which evaluation was based, was made on each writing. The design for this study was an extended factorial analysis. A three way analysis of variance was computed for ability and grade for each level of quality of writing in each mode of discourse. Six hypotheses were tested. Hypotheses one and two dealt with comparison of ratings by students who differed by ability and grade. No significant differences were found. Hypotheses three and four dealt with interaction between grade, ability and mode of discourse. No significant interaction was found. Hypotheses five and six dealt with differences in evaluations between teachers and students of varying ability. A significant difference was found in how teachers and students evaluate writing (p .01). Examination of criteria used in evaluating writings indicated that teachers consistently referred to elements of the text. Students also made text-based comments. In addition, students responded subjectively, referring to common experience, interest, and memories cued by the text.
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James, Sarah. "Please stand if you are able." College Park, Md. : University of Maryland, 2005. http://hdl.handle.net/1903/2499.

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Thesis (M.F.A) -- University of Maryland, College Park, 2005.
Thesis research directed by: Dept. of English. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Books on the topic "Abl2"

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Wurst, Nancy Henderson. Able. New York: Benbella Books, 2009.

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United States. Social Security Administration, ed. Project ABLE: Able beneficiaries' link to employers. [Baltimore, Md.?]: Social Security Administration, 1997.

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Able gate. New York: Dell Books, 1993.

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Monroe, Lucy. And able. New York: Brava/Kensington, 2006.

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Foley, Karen. Able-bodied. Toronto: Harlequin, 2009.

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Sackey, Valerie. Differently able. Accra: Sam-Woode Ltd., 2009.

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Foley, Karen. Able-Bodied. Toronto, Ontario: Harlequin, 2009.

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Bova, Ben. Able one. New York: Tor, 2010.

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Ülker abla. Istanbul: Everest, 2021.

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Hirt, Douglas. Able Gate. [Waterville, Me.]: Wheeler Pub., 2004.

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Book chapters on the topic "Abl2"

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Morris, Christine M., and Suzanne M. Benjes. "BCR-ABL1." In Encyclopedia of Cancer, 1–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_571-3.

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Morris, Christine M., and Suzanne M. Benjes. "BCR-ABL1." In Encyclopedia of Cancer, 460–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_571.

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Russ-Bovelino, Andreas. "carport(able)." In Caramel, 355–60. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0512-2_93.

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Bozalek, Vivienne, and Simone Fullagar. "Able/Disabled." In A Glossary for Doing Postqualitative, New Materialist and Critical Posthumanist Research Across Disciplines, 2–3. London: Routledge, 2021. http://dx.doi.org/10.4324/9781003041153-2.

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Morris, Christine M., and Suzanne M. Benjes. "BCR-ABL1." In Encyclopedia of Cancer, 368–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_571.

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Lüsebrink, Hans-Jürgen. "Farhoud, Abla." In Kindlers Literatur Lexikon (KLL), 1. Stuttgart: J.B. Metzler, 2020. http://dx.doi.org/10.1007/978-3-476-05728-0_11611-1.

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Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "ABL." In Encyclopedia of Molecular Mechanisms of Disease, 2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8901.

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Kinman, Christopher J., Peter Finck, and Lynn Hoffman. "Response-able Practice." In Furthering Talk, 233–51. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-8975-8_14.

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Benger, Kim. "The less able." In School for the Community, 105–10. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003347231-10.

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Bulkeley, Rip. "The Able Seaman." In Bellingshausen and the Russian Antarctic Expedition, 1819–21, 125–40. London: Palgrave Macmillan UK, 2014. http://dx.doi.org/10.1007/978-1-137-40217-2_7.

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Conference papers on the topic "Abl2"

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Hoj, Jacob P., Benjamin J. Mayro, and Ann Marie Pendergast. "Abstract B25: An actionable AXL-ABL2-TAZ signaling axis promotes lung adenocarcinoma metastasis to the brain." In Abstracts: AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; May 8-11, 2019; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-b25.

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Wan, Kenneth W., and Roshan A. Gidwani. "ABLE." In the 30th international. New York, New York, USA: ACM Press, 1993. http://dx.doi.org/10.1145/157485.165034.

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Still, Trent, and Daniel Butko. "Still able." In ICA 2013 Montreal. ASA, 2013. http://dx.doi.org/10.1121/1.4799853.

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"Development of WEB-Based GIS Model Traditional Knowledge in Indonesia Using Soft System Methodology (SSM) and Service Oriented Architecture (SOA)." In ABLE-18, ICLHESS-18 & MLEIS-18. Dignified Researchers Publication (DiRPUB), 2018. http://dx.doi.org/10.15242/dirpub.dirh0118219.

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"Piloting the Expert Learners Seminar Series." In ABLE-18, ICLHESS-18 & MLEIS-18. Dignified Researchers Publication (DiRPUB), 2018. http://dx.doi.org/10.15242/dirpub.dirh0118003.

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"Border Security and Migrant Smuggling: A Study on Illegal Immigrants in the Northern Region in Peninsular of Malaysia." In ABLE-18, ICLHESS-18 & MLEIS-18. Dignified Researchers Publication (DiRPUB), 2018. http://dx.doi.org/10.15242/dirpub.dirh0118006.

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"Web 2.0 tools to Improve Listening and Speaking Skills in a Flipped Classroom." In ABLE-18, ICLHESS-18 & MLEIS-18. Dignified Researchers Publication (DiRPUB), 2018. http://dx.doi.org/10.15242/dirpub.dirh0118008.

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"Status of the Third Gender in India: Comparing the Present with Primeval." In ABLE-18, ICLHESS-18 & MLEIS-18. Dignified Researchers Publication (DiRPUB), 2018. http://dx.doi.org/10.15242/dirpub.dirh0118022.

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"The Use of Apologizing Strategies by College Students." In ABLE-18, ICLHESS-18 & MLEIS-18. Dignified Researchers Publication (DiRPUB), 2018. http://dx.doi.org/10.15242/dirpub.dirh0118027.

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"Traditional Arabic Costume and Indian Salwar Kameez: A Reciprocal Correlation." In ABLE-18, ICLHESS-18 & MLEIS-18. Dignified Researchers Publication (DiRPUB), 2018. http://dx.doi.org/10.15242/dirpub.dirh0118033.

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Reports on the topic "Abl2"

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Meade, Roger. Crossroads Able "Gilda". Office of Scientific and Technical Information (OSTI), August 2020. http://dx.doi.org/10.2172/1647181.

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SCHAFER CORP ALBUQUERQUE NM. ABL Illuminator. Fort Belvoir, VA: Defense Technical Information Center, February 1999. http://dx.doi.org/10.21236/ada361738.

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Yerger, Todd R. Able to Adapt and Conquer. Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada631460.

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Woods, Thomas L. Multilateral Military Operations-Willing and Able? Fort Belvoir, VA: Defense Technical Information Center, March 2011. http://dx.doi.org/10.21236/ada547373.

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Mackey, Greg Edward. Efficient nearest neighbor searches in N-ABLE. Office of Scientific and Technical Information (OSTI), July 2010. http://dx.doi.org/10.2172/992313.

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Schmitt, Mark, Brett Scheiner, Brett Keenan, Derek Schmidt, Lynne Goodwin, Lynn Kot, Kim Molvig, et al. ABLE direct drive multi-shell NIF campaign. Office of Scientific and Technical Information (OSTI), December 2021. http://dx.doi.org/10.2172/1835723.

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Kornbluth, Sally. Inducing Apoptosis in Bcr/Abl-Expressing Cells. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada462025.

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Campbell, Jordan. Throwing Out the Playbook: Insights from the 2021 ABLE Conversation. Creative Generation, March 2022. http://dx.doi.org/10.51163/creative-gen011.

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On Saturday, November 20, 2021, the Berklee Institute for Arts Education and Special Needs (BIAESN) hosted the first ABLE Conversation: Anti-Ableism, Representation, and Accessibility in Arts Education symposium. The event included keynote remarks from Rebecca Cokley and Gaelynn Lea, as well as discussions with attendees. Insights are shared from the event, focused on solidarity work; preparation, access, and opportunity; and the joy of disability culture. It concluded with a strong call to action for the arts education community to be revolutionary and throw out the playbook.
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Erdman, Susan E. Are Anti-Inflammatory Lymphocytes Able to Induce Remission of Breast Cancer. Addendum. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ada468531.

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Williams, Alicia. Do Older Workers Believe They Will Be Able to Retire Comfortably?: Infographic. AARP Research, June 2013. http://dx.doi.org/10.26419/res.00068.002.

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You might also be interested in the extended bibliographies on the topic 'Abl2' for particular source types:
Journal articles Dissertations / Theses Books
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