Global Chromatin Profiling Dataset of Chemical Perturbations in Multiple Biological Backgrounds
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens
SUBMITTER: 
Karen Christianson
PROVIDER: PXD017459 | panorama | Wed Mar 02 00:00:00 GMT 2022
REPOSITORIES: PanoramaPublic
Publications
Proteomic profiling dataset of chemical perturbations in multiple biological backgrounds.
Dele-Oni Deborah O DO Christianson Karen E KE Egri Shawn B SB Vaca Jacome Alvaro Sebastian AS DeRuff Katherine C KC Mullahoo James J Sharma Vagisha V Davison Desiree D Ko Tak T Bula Michael M Blanchard Joel J Young Jennie Z JZ Litichevskiy Lev L Lu Xiaodong X Lam Daniel D Asiedu Jacob K JK Toder Caidin C Officer Adam A Peckner Ryan R MacCoss Michael J MJ Tsai Li-Huei LH Carr Steven A SA Papanastasiou Malvina M Jaffe Jacob D JD
Scientific data 20210825 1
While gene expression profiling has traditionally been the method of choice for large-scale perturbational profiling studies, proteomics has emerged as an effective tool in this context for directly monitoring cellular responses to perturbations. We previously reported a pilot library containing 3400 profiles of multiple perturbations across diverse cellular backgrounds in the reduced-representation phosphoproteome (P100) and chromatin space (Global Chromatin Profiling, GCP). Here, we expand our ...[more]
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To the extent possible under law, all copyright and related or
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and Wnt/?-catenin signaling crosstalk to show the dynamics of
signaling responses during genetic and epigenetic changes in
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results show that cancerous perturbations of components such as
EGFR, Ras, B-Raf, PTEN, and components of the destruction
complex cause extreme fragility in the network and
constitutively activate inter-pathway positive feedback loops.
We observed that the aberrant signaling response due to the
failure of specific network components is transmitted
throughout the network via crosstalk, generating an additive
effect on cancer growth and proliferation.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000656.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
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of genetic or epigenetic alterations, which may lead to
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results show that cancerous perturbations of components such as
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effect on cancer growth and proliferation.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000653.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
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Padala RR, Karnawat R, Viswanathan
SB, Thakkar AV, Das AB.
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of the network such as feedback and feedforward loops.
Perturbation in components within feedback loops causes a
transition from a regulated to a persistently activated state
and results in uncontrolled cell growth. This work represents
the mathematical and quantitative modeling of ERK, PI3K/Akt,
and Wnt/?-catenin signaling crosstalk to show the dynamics of
signaling responses during genetic and epigenetic changes in
cancer. ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk
networks include both intra and inter-pathway feedback loops
which function in a controlled fashion in a healthy cell. Our
results show that cancerous perturbations of components such as
EGFR, Ras, B-Raf, PTEN, and components of the destruction
complex cause extreme fragility in the network and
constitutively activate inter-pathway positive feedback loops.
We observed that the aberrant signaling response due to the
failure of specific network components is transmitted
throughout the network via crosstalk, generating an additive
effect on cancer growth and proliferation.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000654.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000654 | BioModels
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2013-09-19 | E-GEOD-46250 | biostudies-arrayexpress