Evidence map›Paper›PMID 38766216›Full record

ArticlebioRxiv : the preprint server for biology2024

Dual α-globin and truncated EPO receptor knockin restores hemoglobin production in α-thalassemia-derived red blood cells.

Simon N Chu, Eric Soupene, Beeke Wienert, Han Yin, Devesh Sharma, Travis McCreary, Kun Jia, Shota Homma, Jessica P Hampton, James M Gardner and 4 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. 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
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Simon N ChuDepartment of Surgery, University of California, San Francisco, San Francisco, CA.ORCID 0000-0003-3863-1548
Eric SoupeneDepartment of Pediatrics, University of California, San Francisco, Oakland, CA.ORCID 0000-0002-1965-5117
Beeke WienertGladstone Institutes, San Francisco, CA.ORCID 0000-0002-9867-0795
Han YinDepartment of Surgery, University of California, San Francisco, San Francisco, CA.
Devesh SharmaDepartment of Surgery, University of California, San Francisco, San Francisco, CA.
Travis McCrearyDepartment of Surgery, University of California, San Francisco, San Francisco, CA.ORCID 0000-0002-1753-6552
Kun JiaDepartment of Surgery, University of California, San Francisco, San Francisco, CA.
Shota HommaDepartment of Genetics, Stanford University, Stanford, CA.
Jessica P HamptonDepartment of Pediatrics, Stanford University, Stanford, CA.ORCID 0000-0002-0084-5404
James M GardnerDepartment of Surgery, University of California, San Francisco, San Francisco, CA.
Bruce R ConklinGladstone Institutes, San Francisco, CA.ORCID 0000-0003-1463-6061
Tippi C MacKenzieDepartment of Surgery, University of California, San Francisco, San Francisco, CA.ORCID 0000-0001-5232-809X
Matthew H PorteusDepartment of Pediatrics, Stanford University, Stanford, CA.ORCID 0000-0002-3850-4648
M Kyle CromerDepartment of Surgery, University of California, San Francisco, San Francisco, CA.ORCID 0000-0002-8198-5010

Funding

Developing genome editing strategies to treat alpha thalassemiaR01HL161291 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Michael Kyle Cromer, Tippi Mackenzie · 2022 to 2026
$3.6M
C9orf72 frontotemporal dementia (FTD) and amyotrophic lateral sclerosis(ALS): using patient cells and CRISPR to reveal therapeutic approachesRF1AG072052 · NIA · J. DAVID GLADSTONE INSTITUTES · PI CONKLIN, BRUCE R · 2021 to 2022
$2.4M
C9orf72 frontotemporal dementia (FTD) and amyotrophic lateral sclerosis(ALS): using patient cells and CRISPR to reveal therapeutic approachesR01AG072052 · NIA · J. DAVID GLADSTONE INSTITUTES · PI CONKLIN, BRUCE R · 2024 to 2025
$1.4M
NHLBI NIH HHS R01 HL161291NIA NIH HHS R01 AG072052NIA NIH HHS RF1 AG072052
6 · The paper itself

Abstract

Alpha-thalassemia is an autosomal recessive disease with increasing worldwide prevalence. The molecular basis is due to mutation or deletion of one or more duplicated α-globin genes, and disease severity is directly related to the number of allelic copies compromised. The most severe form, α-thalassemia major (αTM), results from loss of all four copies of α-globin and has historically resulted in fatality

Identifiers

PMID38766216
PMCPMC11100611

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.