Evidence map›Paper›PMID 34830113›Full record

ReviewInternational journal of molecular sciences2021

Loss of Function of Mutant IDS Due to Endoplasmic Reticulum-Associated Degradation: New Therapeutic Opportunities for Mucopolysaccharidosis Type II.

Koji Matsuhisa, Kazunori Imaizumi

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

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Genomic Analysis of Abnormal DNAM Methylation in Parathyroid Tumors.International journal of endocrinology · 2022
    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

2 authors at 1 institution in 1 country.

Koji MatsuhisaDepartment of Biochemistry, Institute of Biomedical & Health Sciences, Hiroshima University, Hiroshima 734-8553, Japan.ORCID 0000-0003-0707-9025
Kazunori ImaizumiDepartment of Biochemistry, Institute of Biomedical & Health Sciences, Hiroshima University, Hiroshima 734-8553, Japan.
Hiroshima University · JP

Funding

Japan Society for the Promotion of Science JP17H06416Japan Society for the Promotion of Science JP19K16076Japan Society for the Promotion of Science JP20K21578Satake Technical Foundation NoneTakeda Science Foundation None
6 · The paper itself

Abstract

Mucopolysaccharidosis type II (MPS II) results from the dysfunction of a lysosomal enzyme, iduronate-2-sulfatase (IDS). Dysfunction of IDS triggers the lysosomal accumulation of its substrates, glycosaminoglycans, leading to mental retardation and systemic symptoms including skeletal deformities and valvular heart disease. Most patients with severe types of MPS II die before the age of 20. The administration of recombinant IDS and transplantation of hematopoietic stem cells are performed as therapies for MPS II. However, these therapies either cannot improve functions of the central nervous system or cause severe side effects, respectively. To date, 729 pathogenetic variants in the

Indexed as

Endoplasmic ReticulumEndoplasmic Reticulum-Associated DegradationGlycoproteinsGlycosaminoglycansMucopolysaccharidosis IIMutationHumansMolecular ChaperonesGlycoproteinsGlycosaminoglycansIDS protein, humanMolecular Chaperonesendoplasmic reticulum-associated degradationiduronate-2-sulfataselysosomal storage disordermucopolysaccharidosis type II

Identifiers

PMID34830113
PMCPMC8618218
OpenAlexW3214232272

What Socratic 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 Socratic graph.