Evidence map›Paper›PMID 33517444›Full record

ArticleHuman molecular genetics2021

Genotype & phenotype in Lowe Syndrome: specific OCRL1 patient mutations differentially impact cellular phenotypes.

Swetha Ramadesikan, Lisette Skiba, Jennifer Lee, Kayalvizhi Madhivanan, Daipayan Sarkar, Agustina De La Fuente, Claudia B Hanna, Genki Terashi, Tony Hazbun, Daisuke Kihara and 1 more

Open access · greenAbstract read
In one paragraph

Article in Human molecular genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 18 citations in OpenAlex.

  1. Clinical variation in Lowe syndrome: what and how?Frontiers in cell and developmental biology · 2025
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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

11 authors at 1 institution in 1 country.

Swetha RamadesikanDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
Lisette SkibaDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
Jennifer LeeDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
Kayalvizhi MadhivananDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
Daipayan SarkarDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
Agustina De La FuenteDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
Claudia B HannaDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
Genki TerashiDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
Tony HazbunDepartment of Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, IN 47907, USA.
Daisuke KiharaDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
R Claudio AguilarDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.ORCID 0000-0001-5623-0073
Purdue University West Lafayette · US

Funding

Structural Modeling of Multifarious Protein ComplexesR01GM123055 · NIGMS · PURDUE UNIVERSITY · PI KIHARA, DAISUKE · 2017 to 2020
$1.2M
Lowe Syndrome: Therapeutic Strategy by Drug RepositioningR01DK109398 · NIDDK · PURDUE UNIVERSITY · PI AGUILAR, RUBEN CLAUDIO · 2017 to 2019
$665k
NIDDK NIH HHS R01 DK109398NIGMS NIH HHS R01 GM123055
6 · The paper itself

Abstract

Lowe Syndrome (LS) is a lethal genetic disorder caused by mutations in the OCRL1 gene which encodes the lipid 5' phosphatase Ocrl1. Patients exhibit a characteristic triad of symptoms including eye, brain and kidney abnormalities with renal failure as the most common cause of premature death. Over 200 OCRL1 mutations have been identified in LS, but their specific impact on cellular processes is unknown. Despite observations of heterogeneity in patient symptom severity, there is little understanding of the correlation between genotype and its impact on phenotype. Here, we show that different mutations had diverse effects on protein localization and on triggering LS cellular phenotypes. In addition, some mutations affecting specific domains imparted unique characteristics to the resulting mutated protein. We also propose that certain mutations conformationally affect the 5'-phosphatase domain of the protein, resulting in loss of enzymatic activity and causing common and specific phenotypes (a conformational disease scenario). This study is the first to show the differential effect of patient 5'-phosphatase mutations on cellular phenotypes and introduces a conformational disease component in LS. This work provides a framework that explains symptom heterogeneity and can help stratify patients as well as to produce a more accurate prognosis depending on the nature and location of the mutation within the OCRL1 gene.

Indexed as

Models, MolecularMutationCell LineComputer SimulationHEK293 CellsHumansOculocerebrorenal SyndromePhenotypePhosphoric Monoester HydrolasesProtein ConformationProtein TransportOCRL protein, humanPhosphoric Monoester Hydrolases

Identifiers

PMID33517444
PMCPMC8091038
OpenAlexW3127508442

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.