1. Catalog
  2. Nodes
  3. p(HGNC:ABL1)

p(HGNC:ABL1)

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
ABL1
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 5

Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0

Tau Biochemistry v1.2.5

Tau Biochemistry Section of NESTOR

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Caenorhabditis elegans models of tauopathy v1.0.0

Tau in physiology and pathology v1.0.0

In-Edges 3

a(CHEBI:nilotinib) decreases act(p(HGNC:ABL1)) View Subject | View Object

Inactivation of ABL1 with brain-penetrant nilotinib conferred neuroprotective autophagy in mouse models of PD 153 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
MeSH
Machado-Joseph Disease

path(MESH:"Alzheimer Disease") increases act(p(HGNC:ABL1)) View Subject | View Object

ABL1 is overactivated in AD and tauopathies such as FTD 152 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
MeSH
Machado-Joseph Disease

path(MESH:"Frontotemporal Dementia") increases act(p(HGNC:ABL1)) View Subject | View Object

ABL1 is overactivated in AD and tauopathies such as FTD 152 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
MeSH
Machado-Joseph Disease

Out-Edges 5

p(HGNC:ABL1) decreases bp(GO:macroautophagy) View Subject | View Object

Tyrosine-protein kinase ABL1 is a proto- oncogene that negatively regulates autophagy, partly acting upstream of the RAC serine/threonine-protein kinase (AKT)–mTORC1 axis. PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
MeSH
Machado-Joseph Disease

p(HGNC:ABL1) increases p(HGNC:MAPT, pmod(Ph, Tyr, 394)) View Subject | View Object

Tyrosine kinases target Y18 [fyn, (79)] and Y394 [abl, (31)]. PubMed:17493042

Appears in Networks:
Annotations
Uberon
brain

act(p(HGNC:ABL1), ma(kin)) directlyIncreases p(HGNC:MAPT, pmod(Ph, Tyr, 363)) View Subject | View Object

The single kinase and sequential kinase-catalyzed Fc-phosphorylations points to dramatic changes around the Fc group in the Fc-phosphorylated tau films. Additional surface characterization of the Fc-tau films by time-of-flight secondary ion-mass spectrometry and X-ray photoelectron spectroscopy revealed that Fc-phosphorylations influence the tau orientation and conformation on surfaces. PubMed:23687953

Appears in Networks:

p(HGNC:ABL1) directlyIncreases p(HGNC:MAPT, pmod(Ph, Tyr)) View Subject | View Object

The responsible kinases include 1) proline-directed protein kinases (PDPKs) targeting SP or TP motifs [e.g., GSK3b, cyclindependent kinase (CDK)-5, and MAPKs]; 2) non–proline directed protein kinases targeting KXGS-motifs [e.g., PKA, microtubule affinity-regulating kinase and synapses of the amphid defective (SADK)]; 3) protein kinases specific for tyrosines (e.g., Src, Lck, Syk, Fyn, and c-Abl kinase) (91). PubMed:29191965

Appears in Networks:

p(HGNC:ABL1) directlyIncreases p(HGNC:MAPT, pmod(Ph, Tyr, 394)) View Subject | View Object

In addition, tau can be phosphorylated by tyrosine kinases such as the SRC family members LCK, SYK and FYN at Tyr18, and the ABL family members ARG and ABL1 at Tyr394 (REF. 45). PubMed:26631930

Appears in Networks:

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.