ClinVar Genomic variation as it relates to human health
NM_001099287.2(NIPAL4):c.341C>A (p.Ala114Asp)
The aggregate germline classification for this variant, typically for a monogenic or Mendelian disorder as in the ACMG/AMP guidelines, or for response to a drug. This value is calculated by NCBI based on data from submitters. Read our rules for calculating the aggregate classification.
Stars represent the aggregate review status, or the level of review supporting the aggregate germline classification for this VCV record. This value is calculated by NCBI based on data from submitters. Read our rules for calculating the review status. The number of submissions which contribute to this review status is shown in parentheses.
No data submitted for somatic clinical impact
No data submitted for oncogenicity
Variant Details
- Identifiers
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NM_001099287.2(NIPAL4):c.341C>A (p.Ala114Asp)
Variation ID: 1731 Accession: VCV000001731.31
- Type and length
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single nucleotide variant, 1 bp
- Location
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Cytogenetic: 5q33.3 5: 157468728 (GRCh38) [ NCBI UCSC ] 5: 156895736 (GRCh37) [ NCBI UCSC ]
- Timeline in ClinVar
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First in ClinVar Help The date this variant first appeared in ClinVar with each type of classification.
Last submission Help The date of the most recent submission for each type of classification for this variant.
Last evaluated Help The most recent date that a submitter evaluated this variant for each type of classification.
Germline Apr 4, 2013 Feb 14, 2024 Jan 8, 2024 - HGVS
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Nucleotide Protein Molecular
consequenceNM_001099287.2:c.341C>A MANE Select Help Transcripts from the Matched Annotation from the NCBI and EMBL-EBI (MANE) collaboration.
NP_001092757.2:p.Ala114Asp missense NM_001172292.2:c.284C>A NP_001165763.2:p.Ala95Asp missense NC_000005.10:g.157468728C>A NC_000005.9:g.156895736C>A NG_016626.1:g.13710C>A Q0D2K0:p.Ala176Asp - Protein change
- A176D, A157D, A114D, A95D
- Other names
- p.Ala114Asp
- Canonical SPDI
- NC_000005.10:157468727:C:A
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Functional
consequence HelpThe effect of the variant on RNA or protein function, based on experimental evidence from submitters.
- Unknown function
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Global minor allele
frequency (GMAF) HelpThe global minor allele frequency calculated by the 1000 Genomes Project. The minor allele at this location is indicated in parentheses and may be different from the allele represented by this VCV record.
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0.07488 (G)
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Allele frequency
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The frequency of the allele represented by this VCV record.
1000 Genomes Project 0.00060
The Genome Aggregation Database (gnomAD), exomes 0.00065
Trans-Omics for Precision Medicine (TOPMed) 0.00076
The Genome Aggregation Database (gnomAD) 0.00077
1000 Genomes Project 30x 0.00078
Genes
Gene | OMIM | ClinGen Gene Dosage Sensitivity Curation |
Variation Viewer
Help
Links to Variation Viewer, a genome browser to view variation data from NCBI databases. |
Related variants | ||
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HI score
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The haploinsufficiency score for the gene, curated by ClinGen’s Dosage Sensitivity Curation task team. |
TS score
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The triplosensitivity score for the gene, curated by ClinGen’s Dosage Sensitivity Curation task team. |
Within gene
Help
The number of variants in ClinVar that are contained within this gene, with a link to view the list of variants. |
All
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The number of variants in ClinVar for this gene, including smaller variants within the gene and larger CNVs that overlap or fully contain the gene. |
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NIPAL4 | - | - |
GRCh38 GRCh37 |
155 | 195 |
Conditions - Germline
Condition
Help
The condition for this variant-condition (RCV) record in ClinVar. |
Classification
Help
The aggregate germline classification for this variant-condition (RCV) record in ClinVar. The number of submissions that contribute to this aggregate classification is shown in parentheses. (# of submissions) |
Review status
Help
The aggregate review status for this variant-condition (RCV) record in ClinVar. This value is calculated by NCBI based on data from submitters. Read our rules for calculating the review status. |
Last evaluated
Help
The most recent date that a submitter evaluated this variant for the condition. |
Variation/condition record
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The RCV accession number, with most recent version number, for the variant-condition record, with a link to the RCV web page. |
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Pathogenic (9) |
criteria provided, multiple submitters, no conflicts
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May 13, 2022 | RCV000001801.21 | |
Pathogenic (5) |
criteria provided, multiple submitters, no conflicts
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Jan 8, 2024 | RCV000254897.13 | |
not provided (1) |
no classification provided
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- | RCV001729333.2 | |
Pathogenic (1) |
criteria provided, single submitter
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Apr 11, 2023 | RCV001844003.2 |
Submissions - Germline
Classification
Help
The submitted germline classification for each SCV record. (Last evaluated) |
Review status
Help
Stars represent the review status, or the level of review supporting the submitted (SCV) record. This value is calculated by NCBI based on data from the submitter. Read our rules for calculating the review status. This column also includes a link to the submitter’s assertion criteria if provided, and the collection method. (Assertion criteria) |
Condition
Help
The condition for the classification, provided by the submitter for this submitted (SCV) record. This column also includes the affected status and allele origin of individuals observed with this variant. |
Submitter
Help
The submitting organization for this submitted (SCV) record. This column also includes the SCV accession and version number, the date this SCV first appeared in ClinVar, and the date that this SCV was last updated in ClinVar. |
More information
Help
This column includes more information supporting the classification, including citations, the comment on classification, and detailed evidence provided as observations of the variant by the submitter. |
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Pathogenic
(Apr 07, 2022)
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criteria provided, single submitter
Method: clinical testing
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Autosomal recessive congenital ichthyosis 6
(Autosomal recessive inheritance)
Affected status: yes
Allele origin:
germline
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Foundation for Research in Genetics and Endocrinology, FRIGE's Institute of Human Genetics
Accession: SCV002562747.1
First in ClinVar: Aug 29, 2022 Last updated: Aug 29, 2022 |
Comment:
A homozygous missense variant in exon 4 of the NIPAL4 gene that results in the amino acid substitution of Aspartate for Alanine at codon 114 … (more)
A homozygous missense variant in exon 4 of the NIPAL4 gene that results in the amino acid substitution of Aspartate for Alanine at codon 114 was detected. The observed variant c.341C>A (p.Ala114Asp) has a MAF of 0.05% and 0.07% in the 1000 genomes and gnomAD databases. The in silico prediction of the variant are possibly damaging by PolyPhen-2 (HumDiv) and damaging by LRT and MutationTaster2. The reference codon is conserved across mammals. In summary, the variant meets our criteria to be classified as pathogenic. (less)
Clinical Features:
Ichthyosis (present)
Age: 0-9 years
Sex: male
Method: DNA was used to perform targeted gene capture using a custom capture kit. Libraries were sequenced to mean >80-100X coverage on the Illumina sequencing platform. Sequence obtained were aligned to human references genome using BWA program and analyzed using Picard and GATK-Lite toolkit to identify variants in the targeted genes relevant to clinical indication.
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Pathogenic
(May 26, 2020)
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criteria provided, single submitter
Method: clinical testing
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Autosomal recessive congenital ichthyosis 6
(Autosomal recessive inheritance)
Affected status: yes
Allele origin:
germline
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Victorian Clinical Genetics Services, Murdoch Childrens Research Institute
Additional submitter:
Shariant Australia, Australian Genomics
Accession: SCV002769347.1
First in ClinVar: Dec 24, 2022 Last updated: Dec 24, 2022 |
Comment:
Based on the classification scheme VCGS_Germline_v1.1.1, this variant is classified as Pathogenic. Following criteria are met: 0102 - Loss-of-function is a known mechanism of disease … (more)
Based on the classification scheme VCGS_Germline_v1.1.1, this variant is classified as Pathogenic. Following criteria are met: 0102 - Loss-of-function is a known mechanism of disease for this gene. (N) 0106 - This gene is known to be associated with autosomal recessive disease. (N) 0200 - Variant is predicted to result in a missense amino acid change from alanine to aspartic acid (exon 4). (N) 0252 - Variant is homozygous. (N) 0304 - Variant is present in gnomAD <0.01 for a recessive condition (184 heterozygotes, 0 homozygotes). (P) 0309 - An alternative amino acid change at the same position has been observed in gnomAD (517 heterozygotes, 0 homozygotes). (N) 0501 - Missense variant consistently predicted to be damaging by multiple in silico tools or highly conserved with a major amino acid change. (P) 0600 - Variant is located in an annotated domain or motif (magnesium transporter NIPA domain (PDB, Decipher). (N) 0801 - Strong previous evidence of pathogenicity in unrelated individuals. This variant has been previously reported as one of the most common pathogenic variants in patients with ichthyosis (ClinVar, PMID: 17557927, PMID: 31046801). (P) 1208 - Inheritance information for this variant is not currently available. (N) Legend: (P) - Pathogenic, (N) - Neutral, (B) - Benign (less)
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Pathogenic
(May 13, 2022)
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criteria provided, single submitter
Method: clinical testing
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Autosomal recessive congenital ichthyosis 6
Affected status: unknown
Allele origin:
germline
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Revvity Omics, Revvity
Accession: SCV002018335.3
First in ClinVar: Nov 29, 2021 Last updated: Feb 04, 2024 |
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Pathogenic
(Jan 08, 2024)
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criteria provided, single submitter
Method: clinical testing
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not provided
Affected status: unknown
Allele origin:
germline
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Invitae
Accession: SCV003280699.2
First in ClinVar: Feb 07, 2023 Last updated: Feb 14, 2024 |
Comment:
This sequence change replaces alanine, which is neutral and non-polar, with aspartic acid, which is acidic and polar, at codon 176 of the NIPAL4 protein … (more)
This sequence change replaces alanine, which is neutral and non-polar, with aspartic acid, which is acidic and polar, at codon 176 of the NIPAL4 protein (p.Ala176Asp). This variant is present in population databases (rs199422217, gnomAD 0.1%), and has an allele count higher than expected for a pathogenic variant. This missense change has been observed in individual(s) with autosomal recessive congenital ichthyosis (PMID: 15317751, 17557927, 20016120, 25458912, 26762237, 29444371, 29453417, 31046801, 31168818, 31532840, 34908195, 35412663, 35734965; Invitae). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. It has also been observed to segregate with disease in related individuals. This variant is also known as 341C>A (A114N). ClinVar contains an entry for this variant (Variation ID: 1731). Advanced modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) performed at Invitae indicates that this missense variant is not expected to disrupt NIPAL4 protein function with a negative predictive value of 80%. For these reasons, this variant has been classified as Pathogenic. (less)
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Pathogenic
(Jun 17, 2016)
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criteria provided, single submitter
Method: clinical testing
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not provided
Affected status: unknown
Allele origin:
germline
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Eurofins Ntd Llc (ga)
Accession: SCV000342598.4
First in ClinVar: Dec 06, 2016 Last updated: Dec 15, 2018 |
Number of individuals with the variant: 1
Sex: mixed
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Pathogenic
(Aug 31, 2017)
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criteria provided, single submitter
Method: clinical testing
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Autosomal recessive congenital ichthyosis 6
Affected status: unknown
Allele origin:
germline
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Illumina Laboratory Services, Illumina
Accession: SCV000455918.3
First in ClinVar: Dec 06, 2016 Last updated: May 24, 2019 |
Comment:
The NIPAL4 c.527C>A (p.Ala176Asp) missense variant has been described as one of the two most common pathogenic variants for congenital ichthyosis, together accounting for up … (more)
The NIPAL4 c.527C>A (p.Ala176Asp) missense variant has been described as one of the two most common pathogenic variants for congenital ichthyosis, together accounting for up to 90% of disease alleles (Richard et al. 2014). Across a selection of the available literature, the p.Ala176Asp variant has been identified in a homozygous state in 45 patients and in a compound heterozygous state in eight patients (Lefevre et al. 2004; Dahlqvist et al. 2007; Wajid et al. 2010; Li et al. 2012; Palamar et al. 2015; Kiritsi et al. 2015; Diociaiuti et al. 2016). Up to 60% of individuals were born as collodion babies and most had clinical phenotypes consistent with lamellar ichthyosis or nonbullous congenital ichthyosiform erythroderma. The p.Ala176Asp variant was absent from 300 control chromosomes but is reported at a frequency of 0.0019 in the European American population of the Exome Sequencing Project. Epidermal expression of the ichthyin protein in skin biopsies from healthy individuals showed the enzyme predominantly expressed in the upper epidermis, while expression in individuals homozygous for the p.Ala176Asp variant showed protein in the cell periphery and cytoplasm (Li et al. 2012). Based on the evidence p.Ala176Asp variant is classified as pathogenic for congenital ichthyosis. This variant was observed by ICSL as part of a predisposition screen in an ostensibly healthy population. (less)
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Pathogenic
(Mar 16, 2020)
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criteria provided, single submitter
Method: clinical testing
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Not Provided
Affected status: yes
Allele origin:
germline
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GeneDx
Accession: SCV000321771.8
First in ClinVar: Oct 09, 2016 Last updated: Apr 17, 2019 |
Comment:
The majority of individuals homozygous for this variant present with a collodion membrane at birth and develop generalized ichthyosis with erythema and palmoplantar keratoderma, although … (more)
The majority of individuals homozygous for this variant present with a collodion membrane at birth and develop generalized ichthyosis with erythema and palmoplantar keratoderma, although a lamellar ichthyosis-like phenotype has also been observed (Lefevre et al., 2004); In silico analysis, which includes protein predictors and evolutionary conservation, supports a deleterious effect; This variant is associated with the following publications: (PMID: 25458912, 24397709, 29453417, 31168818, 25525159, 17557927, 20016120, 22622417, 15317751, 22258272, 27025581, 29444371, 26762237, 25326635, 31532840) (less)
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Pathogenic
(Sep 01, 2017)
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criteria provided, single submitter
Method: clinical testing
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Autosomal recessive congenital ichthyosis 6
(Autosomal recessive inheritance)
Affected status: yes
Allele origin:
germline
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Baylor Genetics
Accession: SCV000807612.2
First in ClinVar: Dec 06, 2016 Last updated: Dec 11, 2022 |
Comment:
This variant has been previously reported as disease-causing and was found once in our laboratory homozygous in a 6-month-old female collodion baby with mild micrognathia, … (more)
This variant has been previously reported as disease-causing and was found once in our laboratory homozygous in a 6-month-old female collodion baby with mild micrognathia, microstomia, hypoplastic flexion creases, congenital ichthyosis. Heterozygotes are expected to be asymptomatic carriers. (less)
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Pathogenic
(Apr 11, 2023)
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criteria provided, single submitter
Method: clinical testing
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Lamellar ichthyosis
Affected status: unknown
Allele origin:
germline
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Women's Health and Genetics/Laboratory Corporation of America, LabCorp
Accession: SCV002103582.2
First in ClinVar: Mar 12, 2022 Last updated: Jun 03, 2023 |
Comment:
Variant summary: NIPAL4 c.341C>A (p.Ala114Asp) results in a non-conservative amino acid change in the encoded protein sequence. Five of five in-silico tools predict a damaging … (more)
Variant summary: NIPAL4 c.341C>A (p.Ala114Asp) results in a non-conservative amino acid change in the encoded protein sequence. Five of five in-silico tools predict a damaging effect of the variant on protein function. The variant allele was found at a frequency of 0.00065 in 245384 control chromosomes. This frequency is not significantly higher than estimated for a pathogenic variant in NIPAL4 causing Lamellar Ichthyosis (0.00065 vs 0.001), allowing no conclusion about variant significance. c.341C>A has been reported in the literature in multiple individuals affected with Lamellar Ichthyosis, including several homozygotic individuals (examples: Lefevre_2004, Dahlqvist_2007). These data indicate that the variant is very likely to be associated with disease. To our knowledge, no experimental evidence demonstrating an impact on protein function has been reported. Nine clinical diagnostic laboratories have submitted clinical-significance assessments for this variant to ClinVar after 2014 without evidence for independent evaluation. All laboratories classified the variant as pathogenic/likely pathogenic. Based on the evidence outlined above, the variant was classified as pathogenic. (less)
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Pathogenic
(-)
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criteria provided, single submitter
Method: clinical testing
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Autosomal recessive congenital ichthyosis 6
(Autosomal recessive inheritance)
Affected status: yes
Allele origin:
germline
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Neuberg Centre For Genomic Medicine, NCGM
Accession: SCV004047044.1
First in ClinVar: Oct 28, 2023 Last updated: Oct 28, 2023 |
Comment:
The NIPAL4 c.527C>A (p.Ala176Asp) variant has been reported in heterozygous state in individuals affected with Autosomal recessive congenital ichthyosis (Dalila Maier et al). Experimental studies … (more)
The NIPAL4 c.527C>A (p.Ala176Asp) variant has been reported in heterozygous state in individuals affected with Autosomal recessive congenital ichthyosis (Dalila Maier et al). Experimental studies have shown that this missense decreases the affinity of the NIPAL4 protein (Mauldin EA et al.). This variant has been submitted allele frequency 0.07% in the gnomAD and novel in 1000 genome database. It has been submitted to ClinVar as pathogenic. The amino acid Ala at position 176 is changed to a Asp changing protein sequence and it might alter its composition and physico-chemical properties. The amino acid change p.Ala176Asp in NIPAL4 is predicted as conserved by GERP++ and PhyloP across 100 vertebrates. For these reasons, this variant has been classified as Pathogenic (less)
Clinical Features:
Ichthyosis (present) , Congenital ichthyosiform erythroderma (present)
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Pathogenic
(May 16, 2019)
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no assertion criteria provided
Method: clinical testing
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Autosomal recessive congenital ichthyosis 6
Affected status: yes
Allele origin:
germline
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Institute for Human Genetics, University Medical Center Freiburg
Accession: SCV000930510.1
First in ClinVar: Aug 05, 2019 Last updated: Aug 05, 2019 |
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Likely pathogenic
(-)
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no assertion criteria provided
Method: clinical testing
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not provided
Affected status: yes
Allele origin:
germline
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Joint Genome Diagnostic Labs from Nijmegen and Maastricht, Radboudumc and MUMC+
Additional submitter:
Diagnostic Laboratory, Department of Genetics, University Medical Center Groningen
Study: VKGL Data-share Consensus
Accession: SCV001958700.1 First in ClinVar: Oct 02, 2021 Last updated: Oct 02, 2021 |
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Likely pathogenic
(-)
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no assertion criteria provided
Method: clinical testing
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not provided
Affected status: yes
Allele origin:
germline
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Clinical Genetics DNA and cytogenetics Diagnostics Lab, Erasmus MC, Erasmus Medical Center
Additional submitter:
Diagnostic Laboratory, Department of Genetics, University Medical Center Groningen
Study: VKGL Data-share Consensus
Accession: SCV001973200.1 First in ClinVar: Oct 07, 2021 Last updated: Oct 07, 2021 |
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Pathogenic
(Oct 01, 2007)
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no assertion criteria provided
Method: literature only
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ICHTHYOSIS, CONGENITAL, AUTOSOMAL RECESSIVE 6
Affected status: not provided
Allele origin:
germline
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OMIM
Accession: SCV000021957.2
First in ClinVar: Apr 04, 2013 Last updated: Apr 30, 2023 |
Comment on evidence:
In a study of 27 patients from 18 families with autosomal recessive congenital ichthyosis-6 (612281) characterized by electron microscopy (EM) as type III (ARCI EM … (more)
In a study of 27 patients from 18 families with autosomal recessive congenital ichthyosis-6 (612281) characterized by electron microscopy (EM) as type III (ARCI EM type III), with abnormal lamellar bodies in stratum granulosum and perinuclear, elongated membranes, Dahlqvist et al. (2007) found a 527C-to-A transversion in exon 4 of the NIPAL4 cDNA that led to an ala176-to-asp (A176D) amino acid substitution. The mutation was found in 37 of the 54 alleles examined. (less)
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Pathogenic
(-)
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no assertion criteria provided
Method: clinical testing
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Autosomal recessive congenital ichthyosis 6
Affected status: yes
Allele origin:
germline
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Genomics England Pilot Project, Genomics England
Accession: SCV001760158.1
First in ClinVar: Jul 31, 2021 Last updated: Jul 31, 2021 |
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not provided
(-)
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no classification provided
Method: literature only
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Autosomal recessive congenital ichthyosis
Affected status: unknown
Allele origin:
germline
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GeneReviews
Accession: SCV001980663.2
First in ClinVar: Oct 16, 2021 Last updated: Oct 01, 2022 |
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Germline Functional Evidence
Functional
Help
The functional consequence of the variant, based on experimental evidence and provided by the submitter. consequence |
Method
Help
A brief description of the method used to determine the functional consequence of the variant. A citation for the method is included, when provided by the submitter. |
Result
Help
A brief description of the result of this method for this variant. |
Submitter
Help
The submitting organization for this submitted (SCV) record. This column also includes the SCV accession and version number, the date this SCV first appeared in ClinVar, and the date that this SCV was last updated in ClinVar. |
More information
Help
This column includes more information supporting functional evidence for the germline classification, including citations, the comment on classification, and detailed evidence provided as observations of the variant by the submitter. |
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Unknown function
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Foundation for Research in Genetics and Endocrinology, FRIGE's Institute of Human Genetics
Accession: SCV002562747.1
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Citations for germline classification of this variant
HelpTitle | Author | Journal | Year | Link |
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Autosomal Recessive Congenital Ichthyosis. | Adam MP | - | 2023 | PMID: 20301593 |
Genetic Etiology of Ichthyosis in Turkish Patients: Next-generation Sequencing Identified Seven Novel Mutations. | Saat H | Medeniyet medical journal | 2022 | PMID: 35734965 |
Genotype of autosomal recessive congenital ichthyosis from a tertiary care center in India. | Chiramel MJ | Pediatric dermatology | 2022 | PMID: 35412663 |
Quality of life and clinical characteristics of self-improving congenital ichthyosis within the disease spectrum of autosomal-recessive congenital ichthyosis. | Hake L | Journal of the European Academy of Dermatology and Venereology : JEADV | 2022 | PMID: 34908195 |
Genotype-phenotype correlation in a large English cohort of patients with autosomal recessive ichthyosis. | Simpson JK | The British journal of dermatology | 2020 | PMID: 31168818 |
Autosomal recessive congenital ichthyosis due to homozygous variants in NIPAL4 with a dramatic response to ustekinumab. | Poulton C | Pediatric dermatology | 2019 | PMID: 31532840 |
Inherited ichthyoses: molecular causes of the disease in Czech patients. | Borská R | Orphanet journal of rare diseases | 2019 | PMID: 31046801 |
Exome sequencing has higher diagnostic yield compared to simulated disease-specific panels in children with suspected monogenic disorders. | Dillon OJ | European journal of human genetics : EJHG | 2018 | PMID: 29453417 |
Whole-exome sequencing for diagnosis of hereditary ichthyosis. | Sitek JC | Journal of the European Academy of Dermatology and Venereology : JEADV | 2018 | PMID: 29444371 |
Role of molecular testing in the multidisciplinary diagnostic approach of ichthyosis. | Diociaiuti A | Orphanet journal of rare diseases | 2016 | PMID: 26762237 |
Whole-exome sequencing in patients with ichthyosis reveals modifiers associated with increased IgE levels and allergic sensitizations. | Kiritsi D | The Journal of allergy and clinical immunology | 2015 | PMID: 25458912 |
Genotype and Anterior Segment Phenotype in a Cohort of Turkish Patients with Lamellar Ichthyosis. | Palamar M | Ophthalmic genetics | 2015 | PMID: 24397709 |
The expression of epidermal lipoxygenases and transglutaminase-1 is perturbed by NIPAL4 mutations: indications of a common metabolic pathway essential for skin barrier homeostasis. | Li H | The Journal of investigative dermatology | 2012 | PMID: 22622417 |
NIPAL4/ichthyin is expressed in the granular layer of human epidermis and mutated in two Pakistani families with autosomal recessive ichthyosis. | Wajid M | Dermatology (Basel, Switzerland) | 2010 | PMID: 20016120 |
Autosomal recessive congenital ichthyosis. | Fischer J | The Journal of investigative dermatology | 2009 | PMID: 19434086 |
Congenital ichthyosis: mutations in ichthyin are associated with specific structural abnormalities in the granular layer of epidermis. | Dahlqvist J | Journal of medical genetics | 2007 | PMID: 17557927 |
Mutations in ichthyin a new gene on chromosome 5q33 in a new form of autosomal recessive congenital ichthyosis. | Lefèvre C | Human molecular genetics | 2004 | PMID: 15317751 |
http://www.egl-eurofins.com/emvclass/emvclass.php?approved_symbol=NIPAL4 | - | - | - | - |
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Text-mined citations for rs199422217 ...
HelpRecord last updated Apr 06, 2024
This date represents the last time this VCV record was updated. The update may be due to an update to one of the included submitted records (SCVs), or due to an update that ClinVar made to the variant such as adding HGVS expressions or a rs number. So this date may be different from the date of the “most recent submission” reported at the top of this page.