Article in Methods in enzymology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.0field-weighted citation impact, top 28% of its field
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literature
Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
4 authors at 1 institution in 1 country.
Arthur ChowDepartment of Oncological Sciences, Department of Pharmacological Sciences, The Tisch Cancer Institute, Mount Sinai Centre for Therapeutic Discovery, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Zaigham M KhanDepartment of Oncological Sciences, Department of Pharmacological Sciences, The Tisch Cancer Institute, Mount Sinai Centre for Therapeutic Discovery, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
William M MarsigliaDepartment of Oncological Sciences, Department of Pharmacological Sciences, The Tisch Cancer Institute, Mount Sinai Centre for Therapeutic Discovery, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Arvin C DarDepartment of Oncological Sciences, Department of Pharmacological Sciences, The Tisch Cancer Institute, Mount Sinai Centre for Therapeutic Discovery, Icahn School of Medicine at Mount Sinai, New York, NY, United States. Electronic address: arvin.dar@mssm.edu.
Icahn School of Medicine at Mount Sinai · US
Funding
THE TISCH CANCER INSTITUTE - CANCER CENTER SUPPORT GRANTP30CA196521 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Ramon E Parsons · 2015 to 2026
$35.4M
TRAINING PROGRAM IN CANCER THERAPYT32CA078207 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI James J Manfredi · 1999 to 2026
$11.6M
Targeting Oncogenic Ras-MAPK Signaling Complexes via the Scaffold KSRR01CA227636 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Arvin Dar · 2018 to 2026
$4.0M
AN INTEGRATED PLATFORM FOR NOVEL PERSONALIZED LIVER CANCER THERAPEUTICSR01CA256480 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI DAR, ARVIN, GUCCIONE, ERNESTO · 2021 to 2025
$3.3M
A Chemical Genetic Approach to Exploring Novel Therapeutic Space for Colorectal CancerR01CA258736 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI DAR, ARVIN · 2021 to 2025
$3.2M
A Cytochrome P450 Therapeutic Space for TauopathiesR56AG066712 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CAGAN, ROSS LEIGH, DAR, ARVIN · 2021 to 2021
$802k
Defining the relationship between kinase inhibitor pharmacophores and pro-/anti-targets using in vivo models of colorectal cancerK00CA212474 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MARSIGLIA, WILLIAM M · 2019 to 2022
$374k
Mechanisms of resistance and activation conferred by kinases displaying hinge and gate-keeper mutationsF99CA212474 · NCI · NEW YORK UNIVERSITY · PI MARSIGLIA, WILLIAM M · 2016 to 2017
Pseudokinases often operate through functionally related enzymes and receptors. A prime example is the pseudokinase KSR (Kinase Suppressor of RAS), which can act as both an amplifier and inhibitor of members in the RAS-MAPK (Mitogen Activated Protein Kinase) signaling pathway. KSR is structurally related to the active RAF kinases over multiple domains; moreover, the pseudokinase domain of KSR forms physical and regulatory complexes with both RAF and MEK through distinct interfaces. Characterization of small molecule interactions on KSR has been used to uncover novel chemical tools and understand the mechanism of action of clinical drugs. Here, we elaborate on assays and structural methods for measuring binding at orthosteric and interfacial binding sites on KSR. These distinct small molecule pockets provide therapeutic paths for targeting KSR1 and KSR2 pseudokinases in disease, including in RAS and RAF mutant cancers.
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Conformational control and regulation of the pseudokinase KSR via small molecule binding interactions. · full record | OpenQuestion