human ABL1 shRNA silencing Adenovirus

Abelson murine leukemia viral oncogene homolog 1; Abelson tyrosine-protein kinase 1; ABL; bcr/abl; bcr/c-abl oncogene protein; c-ABL; c-abl oncogene 1, receptor tyrosine kinase; c-ABL1; CHDSKM; JTK7; p150; proto-oncogene c-Abl; proto-oncogene tyrosine-protein kinase ABL1; tyrosine-protein kinase ABL1; v-abl; v-abl Abelson murine leukemia viral oncogene homolog 1

c-Abl is the human cellular homolog of a the v-Abl viral oncogene. v-Abl was originally discovered as a mouse cell-derived sequence in the genome of the Abelson murine leukemia virus (A-MuLV), a transforming retrovirus isolated by the laboratory of Dr. H.T. Abelson. c-Abl is a tyrosine kinase from the Src-family of tyrosine kinases that localizes to both the cytoplasm and nucleus. It bears an SH2 (src-homology 2) and SH3 (src-homology 3) domain responsible for mediating c-Abl protein-protein interactions. c-Abl is implicated to play a role in multiple cellular processes such as cell cycle checkpoint signaling, apoptosis, cell differentiation, cell adhesion, and transcriptional regulation. Chromosomal translocations involving the c-Abl gene are associated with human leukemias.

The ABL1 protooncogene encodes a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell differentiation, cell division, cell adhesion, and stress response. Activity of c-Abl protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns ABL1 into an oncogene. The t(9;22) translocation results in the head-to-tail fusion of the BCR (MIM:151410) and ABL1 genes present in many cases of chronic myelogeneous leukemia. The DNA-binding activity of the ubiquitously expressed ABL1 tyrosine kinase is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function for ABL1. The ABL1 gene is expressed as either a 6- or 7-kb mRNA transcript, with alternatively spliced first exons spliced to the common exons 2-11.

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ABL proto-oncogene 1, non-receptor tyrosine kinase

ABL proto-oncogene 1, non-receptor tyrosine kinase

ABL1

HGNC:76

9606.0

3450

3450 bp

Tyrosine-protein kinase ABL1

NM_007313

NM_007313, NM_005157, BC117451,

Apoptosis,Autophagy,Axon Guidance,Breast Cancer,Cancer,Cardiology,Cardiovascular,Cell Cycle,Cytoskeleton,DNA Damage/Repair,EGFR Signaling,Homologous Recombination,Host-Virus Interactions,Immunology,Innate Immunity,Kinase/Phosphatase,Leukemia,MicroRNAs in Cancer,Mitochondrion,Neurobiology,Neurodevelopment,p53 Signaling,PDGF Signaling,SCF-KIT Signaling,Signal Transduction,T-cell Receptor Signaling,Transcription Factor/Regulator,Translational Control

cancer,cardiovascular,cell_biology,cell_cycle,developmental_biology,genetics,immunology,infectious_disease,neurobiology,signal_transduction,stem_cell_biology,transcription_translation

human

c-Abl is the human cellular homolog of a the v-Abl viral oncogene. v-Abl was originally discovered as a mouse cell-derived sequence in the genome of the Abelson murine leukemia virus (A-MuLV), a transforming retrovirus isolated by the laboratory of Dr. H.T. Abelson. c-Abl is a tyrosine kinase from the Src-family of tyrosine kinases that localizes to both the cytoplasm and nucleus. It bears an SH2 (src-homology 2) and SH3 (src-homology 3) domain responsible for mediating c-Abl protein-protein interactions. c-Abl is implicated to play a role in multiple cellular processes such as cell cycle checkpoint signaling, apoptosis, cell differentiation, cell adhesion, and transcriptional regulation. Chromosomal translocations involving the c-Abl gene are associated with human leukemias.

Hs.431048

P00519