Evidence map›Paper›PMID 35892570›Full record

ArticleCells2022

SLC35A2 Deficiency Promotes an Epithelial-to-Mesenchymal Transition-like Phenotype in Madin-Darby Canine Kidney Cells.

Magdalena Kot, Ewa Mazurkiewicz, Maciej Wiktor, Wojciech Wiertelak, Antonina Joanna Mazur, Andrei Rahalevich, Mariusz Olczak, Dorota Maszczak-Seneczko

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Disrupted O-GalNAc glycosylation as a mechanism and biomarker ofbioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Review
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

8 authors at 1 institution in 1 country.

Magdalena KotDepartment of Cell Pathology, Faculty of Biotechnology, University of Wroclaw, 14A F. Joliot-Curie St., 50-383 Wroclaw, Poland.ORCID 0000-0001-8374-2090
Ewa MazurkiewiczDepartment of Cell Pathology, Faculty of Biotechnology, University of Wroclaw, 14A F. Joliot-Curie St., 50-383 Wroclaw, Poland.ORCID 0000-0002-5418-5712
Maciej WiktorDepartment of Biochemistry, Faculty of Biotechnology, University of Wroclaw, 14A F. Joliot-Curie St., 50-383 Wroclaw, Poland.ORCID 0000-0001-9606-1841
Wojciech WiertelakDepartment of Biochemistry, Faculty of Biotechnology, University of Wroclaw, 14A F. Joliot-Curie St., 50-383 Wroclaw, Poland.ORCID 0000-0002-6716-0696
Antonina Joanna MazurDepartment of Cell Pathology, Faculty of Biotechnology, University of Wroclaw, 14A F. Joliot-Curie St., 50-383 Wroclaw, Poland.ORCID 0000-0002-7561-9030
Andrei RahalevichDepartment of Biochemistry, Faculty of Biotechnology, University of Wroclaw, 14A F. Joliot-Curie St., 50-383 Wroclaw, Poland.
Mariusz OlczakDepartment of Biochemistry, Faculty of Biotechnology, University of Wroclaw, 14A F. Joliot-Curie St., 50-383 Wroclaw, Poland.ORCID 0000-0001-8629-6364
Dorota Maszczak-SeneczkoDepartment of Biochemistry, Faculty of Biotechnology, University of Wroclaw, 14A F. Joliot-Curie St., 50-383 Wroclaw, Poland.ORCID 0000-0002-5112-7920
University of Wrocław · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In mammalian cells, SLC35A2 delivers UDP-galactose for galactosylation reactions that take place predominantly in the Golgi lumen. Mutations in the corresponding gene cause a subtype of a congenital disorder of glycosylation (SLC35A2-CDG). Although more and more patients are diagnosed with SLC35A2-CDG, the link between defective galactosylation and disease symptoms is not fully understood. According to a number of reports, impaired glycosylation may trigger the process of epithelial-to-mesenchymal transition (EMT). We therefore examined whether the loss of SLC35A2 activity would promote EMT in a non-malignant epithelial cell line. For this purpose, we knocked out the

Indexed as

Epithelial-Mesenchymal TransitionKidneyAnimalsDogsMadin Darby Canine Kidney CellsMammalsPhenotypeVimentinVimentincongenital disorder of glycosylation (CDG)epithelial-to-mesenchymal transition (EMT)fibronectinglycosylationGolgi complexMadin–Darby canine kidney (MDCK) cellsmigrationsolute carrier family 35 member A2 (SLC35A2)UDP-galactosevimentin

Identifiers

PMID35892570
PMCPMC9331475
OpenAlexW4287009901

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.