Evidence map›Paper›PMID 34368857›Full record

ArticleMolecular medicine reports2021

Functional study of SCCD pathogenic gene

Jumin Xie, Lingxing Li

Abstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. 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

2 authors.

Jumin XieMedical School of Renal Disease Occurrence and Intervention, Hubei Polytechnic University, Huangshi, Hubei 435003, P.R. China.
Lingxing LiDepartment of Cardiovascular Medicine, Tai'an City Central Hospital, Tai'an, Shandong 271000, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schnyder's crystalline corneal dystrophy (SCCD) is a rare autosomal dominant genetic disorder that is characterized by progressive corneal opacity, owing to aberrant accumulation of cholesterol and phospholipids in the cornea. A number of SCCD affected families have been reported in the world since 1924, when it was first described. In 2007, the molecular basis of SCCD was demonstrated to be associated with a tumor suppressor, UbiA prenyltransferase domain‑containing 1 (UBIAD1), which was isolated from the bladder mucosa and demonstrated to be involved in vitamin K

Indexed as

AnimalsCholesterolCorneaCorneal Dystrophies, HereditaryDimethylallyltranstransferaseEndoplasmic ReticulumGenes, Tumor SuppressorGenetic Predisposition to DiseaseHumansMutationPolyisoprenyl PhosphatesVitamin K 2CholesterolDimethylallyltranstransferasegeranylgeranyl pyrophosphatePolyisoprenyl PhosphatesUBIAD1 protein, humanVitamin K 23‑hydroxy‑3‑methyl‑glutaryl coenzyme A reductasecholesterol biosynthesisER‑associated degradationSchnyder's crystalline corneal dystrophyUbiA Prenyltransferase Domain Containing 1

Identifiers

PMID34368857
PMCPMC8365407

What OpenQuestion holds

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Registered trials

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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.