ShcA expression in podocytes is dispensable for glomerular development but its upregulation is associated with kidney disease.

Claire E Martin, Nina Jones

Open access · greenAbstract read

In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

0.1field-weighted citation impact, top 50% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

2 authors at 1 institution in 1 country.

Claire E MartinDepartment of Molecular and Cellular Biology, University of Guelph Guelph, ON, Canada.

Nina JonesDepartment of Molecular and Cellular Biology, University of Guelph Guelph, ON, Canada.

University of Guelph · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundShcA (

methodsWe selectively deleted all three isoforms of ShcA from mouse kidney podocytes using the Cre/lox system driven by the podocyte-specific podocin promoter (

resultsMice lacking podocyte ShcA were born at the expected Mendelian frequency and did not display overt renal impairment or changes in podocyte architecture beyond one year of age. In parallel, we correlated increased ShcA mRNA expression in the human kidney with proteinuria and reduced glomerular filtration rate.

conclusionOur studies reveal that ShcA is dispensable for normal kidney function, but its upregulation is associated with disease.

Indexed as

glomerulusknockout miceNephroseqpodocyteShcA

Identifiers

PMID34540124

PMCPMC8430102

OpenAlexW3200050055

What Socratic holds

Textmetadata

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 Socratic graph.