Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Activating KRAS, NRAS, and BRAF mutants enhance proteasome capacity and reduce endoplasmic reticulum stress in multiple myeloma.

Proceedings of the National Academy of Sciences of the United States of America - 18 Aug 2020

Shirazi Fazal, Jones Richard J, Singh Ram K, Zou Jianxuan, Kuiatse Isere, Berkova Zuzana, Wang Hua, Lee Hans C, Hong Samuel, Dick Larry, Chattopadhyay Nibedita, Orlowski Robert Z

Abstract excerpt

KRAS, NRAS, and BRAF mutations which activate p44/42 mitogen-activated protein kinase (MAPK) signaling are found in half of myeloma patients and contribute to proteasome inhibitor (PI) resistance, but the underlying mechanisms are not fully understood. We established myeloma cell lines expressing wild-type (WT), constitutively active (CA) (G12V/G13D/Q61H), or dominant-negative (DN) (S17N)-KRAS and -NRAS, or...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Apoptosis
Share to GTP Phosphohydrolases

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Membrane Proteins

Share to Multiple Myeloma

Share to Mutation

Share to Protein Kinase Inhibitors

Share to Proto-Oncogene Proteins B-raf

Share to Proto-Oncogene Proteins p21(ras)

Source

Open in PubMed Open full text

Identifiers

PMID: 32747568
DOI: 10.1073/pnas.2005052117
PMCID: PMC7443929

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Activating KRAS, NRAS, and BRAF mutants enhance proteasome capacity and reduce endoplasmic reticulum stress in multiple myeloma.PMID 32747568Read ↗

Molecular mechanisms in multiple myeloma drug resistance.Semantic proximity Read ↗

Pathway-Directed Therapy in Multiple MyelomaSemantic proximity Read ↗

<em>KRAS/NRAS</em> Mutation-Associated Transcriptional Dysregulation Identifies <em>NRL</em>, <em>CREM </em>and <em>IL-6</em> as Candidate Prognostic Biomarkers in Multiple MyelomaSemantic proximity Read ↗

Endoplasmic reticulum stress in the development of multiple myeloma and drug resistanceSemantic proximity Read ↗

The p97 Inhibitor CB-5083 Is a Unique Disrupter of Protein Homeostasis in Models of Multiple MyelomaSemantic proximity Read ↗

The proteasome: mechanisms of biology and markers of activity and response to treatment in multiple myelomaSemantic proximity Read ↗

The Landscape of Signaling Pathways and Proteasome Inhibitors Combinations in Multiple MyelomaSemantic proximity Read ↗

Integrated phosphoproteomics and transcriptional classifiers reveal hidden RAS signaling dynamics in multiple myeloma.Semantic proximity Read ↗

Different Strategies to Overcome Resistance to Proteasome Inhibitors—A Summary 20 Years after Their IntroductionSemantic proximity Read ↗

Oncogenic RAS commandeers amino acid sensing machinery to aberrantly activate mTORC1 in multiple myeloma.Semantic proximity Read ↗

Phosphoinositide Protein Kinase PDPK1 Is a Crucial Cell Signaling Mediator in Multiple MyelomaSemantic proximity Read ↗

Emerging therapies targeting the ubiquitin proteasome system in cancerSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.