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Record W2326935077 · doi:10.1158/1538-7445.am10-1234

Abstract 1234: Erk-dependent phosphorylation of Notch intracellular domain (NIC) correlates with increased NIC-dependent transcription

2010· article· en· W2326935077 on OpenAlex
Isabelle Tremblay, Marie‐Josée Boucher

Why this work is in the frame

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

affAt least one author lists a Canadian institution in the pinned OpenAlex snapshot.

Bibliographic record

VenueCancer Research · 2010
Typearticle
Languageen
FieldMedicine
TopicCancer Mechanisms and Therapy
Canadian institutionsUniversité de Sherbrooke
Fundersnot available
KeywordsMAPK/ERK pathwayHES1MEK inhibitorTransfectionMolecular biologyLuciferaseTranscription factorChemistryTranscription (linguistics)KRASNotch signaling pathwayCell biologyPhosphorylationBiologyCancer researchSignal transductionBiochemistryGeneMutation

Abstract

fetched live from OpenAlex

Abstract Background. Recent studies have suggested that the ability of Ras to transform cells depends on cooperation with the Notch signaling pathway. However, the molecular and cellular mechanisms involved in this cooperation remain unknown. Aim. To evaluate the impact of the Mek/Erk pathway, downstream of Ras, on Notch signaling. Methods. HEK293T and human pancreatic cancer cells MIA PaCa-2 were used. Mek/Erk activity was down-regulated by treatment with the specific inhibitor U0126 (10 µM). Transfections or retroviral infections of a constitutive active form of KRas or Mek (MekCA) were used to increase Mek/Erk activity. NIC-dependent transcription was measured by luciferase assays using a specific (CSL) luciferase reporter gene. Results. 1- Transient transfection of an activated KRas stimulated by 1.7-fold NIC-dependent transcription. Transfection of MekCA increased by 4.3-fold NIC-dependent transcription while a wild-type form of Mek (MekWT) was without effect. In parallel, treatment with U0126 reduced by 60% the basal NIC-dependent transcription and completely blocked the KRas- and MekCA-induced NIC-dependent transcription. This negative effect of U0126 on NIC-dependent transcription correlated with decreased nuclear staining of the NIC target gene Hes1. 2- Western blot analysis revealed higher molecular weight forms of NIC when cells were transfected/infected with MekCA as compared to control MekWT-transfected/infected cells. U0126 treatment prevented the MekCA-induced decreased in mobility shift of NIC suggesting that NIC is subjected to Mek-dependent post-translational modifications in vivo. 3- Immunoprecipitation followed by in vitro phosphatase assay revealed that these MekCA-induced higher molecular weight forms of NIC were phosphorylated forms of NIC. 4- By in vitro kinase assays, we demonstrated that NIC worked as Erk substrate. 5- Finally, following in vivo phospholabeling, we observed that NIC immunoprecipitated from MekCA-transfected cells was more phosphorylated as compared to NIC immunoprecipitated from MekWT-transfected cells. Conclusion. Our results provide the novel discovery that Mek/Erk signaling promotes NIC phosphorylation which correlates with increased NIC-dependent transcription. Our discovery thus provides a possible cellular mechanism by which Ras and Notch cooperate to promote cellular transformation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1234.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.002
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesInsufficient payload (model declined to judge)
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.011
Threshold uncertainty score0.997

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0020.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0040.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.030
GPT teacher head0.330
Teacher spread0.300 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it