Evidence map›Paper›PMID 36618440›Full record

ArticleAdvanced genetics (Hoboken, N.J.)2021

Embryonic lethality and defective mammary gland development of activator-function impaired conditional knock-in

Kate Senger, Wenlin Yuan, Meredith Sagolla, Jonas Doerr, Brad Bolon, James Ziai, Kai-Hui Sun, Soren Warming, Merone Roose-Girma, Na Zhang and 10 more

Open access · goldAbstract read
In one paragraph

Article in Advanced genetics (Hoboken, N.J.), 2021. 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
0.2field-weighted citation impact, top 46% 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, 3 citations in OpenAlex.

  1. Article
  2. Article
4 · The record

Corrections and comments

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

20 authors at 5 institutions in 3 countries.

Kate SengerDepartment of Molecular Biology Genentech South San Francisco California USA.
Wenlin YuanDepartment of Molecular Biology Genentech South San Francisco California USA.
Meredith SagollaDepartment of Pathology Genentech South San Francisco California USA.
Jonas DoerrDepartment of Molecular Biology Genentech South San Francisco California USA.
Brad BolonGEMpath Inc. Longmont Colorado USA.
James ZiaiDepartment of Pathology Genentech South San Francisco California USA.
Kai-Hui SunDepartment of Molecular Biology Genentech South San Francisco California USA.
Soren WarmingDepartment of Molecular Biology Genentech South San Francisco California USA.
Merone Roose-GirmaDepartment of Molecular Biology Genentech South San Francisco California USA.
Na ZhangDepartment of Molecular Biology Genentech South San Francisco California USA.
Lucinda TamDepartment of Molecular Biology Genentech South San Francisco California USA.
Robert J NewmanDepartment of Molecular Biology Genentech South San Francisco California USA.
Subhra ChaudhuriDepartment of Molecular Biology Genentech South San Francisco California USA.
Aju AntonySciGenom Labs Pvt Ltd Kochi Kerala India.
Leonard D GoldsteinDepartment of Bioinformatics and Computational Biology Genentech South San Francisco California USA.
Steffen DurinckDepartment of Bioinformatics and Computational Biology Genentech South San Francisco California USA.
Bijay S JaiswalDepartment of Molecular Biology Genentech South San Francisco California USA.
Daniel LafkasDepartment of Immunology Discovery Genentech South San Francisco California USA.
Zora ModrusanDepartment of Molecular Biology Genentech South San Francisco California USA.
Somasekar SeshagiriDepartment of Molecular Biology Genentech South San Francisco California USA.ORCID https://orcid.org/0000-0003-4272-6443
Gene Therapy Laboratory · FRInstitut thématique Génétique, génomique et bioinformatique · FRKaiser Permanente South San Francisco Medical Center · USNewPath Research · USSciGenom Labs (India) · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ERBB3 is a pseudokinase domain-containing member of the ERBB family of receptor tyrosine kinases (RTKs). Following ligand binding, ERBB receptors homo- or hetero-dimerize, leading to a head-to-tail arrangement of the intracellular kinase domains, where the "receiver" kinase domain of one ERBB is activated by the "activator" domain of the other ERBB in the dimer. In ERBB3, a conserved valine at codon 943 (V943) in the kinase C-terminal domain has been shown to be important for its function as an "activator" kinase

Indexed as

animal geneticsbasic medical sciencesdevelopmental geneticsgeneticsgenetics or genomicsmedicinemolecular medicine

Identifiers

PMID36618440
PMCPMC9744554
OpenAlexW3110483402

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.