11 Matching Annotations
  1. Oct 2026
    1. Unusual OCT findings in a patient with CABP4-associated cone-rod synaptic disorder

      PMID: 38206458

      Gene: CABP4

      HGNC: 1386

      Disease: cone-rod synaptic disorder, congenital nonprogressive

      MONDO: 0012490

      InheritancePattern: autosomal recessive

      Prevalence: The prevalence of the Åland eye disease or incomplete congenital stationary night blindness phenotype was estimated at 1 in 22,000 based on a Danish male cohort, with CABP4 variants specifically responsible for 1 out of 35 cases (PMID: 28002560).

      Penetrance: Penetrance appears to be 100% among the reported individuals harboring biallelic disease-causing CABP4 variants.

    1. Homozygosity mapping was performed in a consanguineous family with four affected members originally referred as cases of LCA. Detailed electroretinographic recordings were obtained. Results: A novel homozygous single base-pair insertion was identified in all four siblings. The patients had an LCA-like phenotype, including either flat or greatly diminished electroretinographic activity. Conclusions: This report significantly expands on the phenotype associated with calcium binding protein 4 mutations, which has so far been limited to congenital stationary night blindness, and further demonstrates how molecular data often blur the boundaries between what are believed to be clinically distinct retinal disorders.

      Case#: Aldahmesh_2010_Family_Proband_II-1, male, onset in early childhood, age 12 years at time of report, family ancestry reported as Dutch

      CasePresentingHPOs: HP:0011463 (Childhood onset), HP:0000639 (Nystagmus), HP:0007663 (Reduced visual acuity), HP:0000613 (Photophobia), HP:0000551 (Color vision defect)

      CaseHPOFreeText: The proband and his sibling have a diagnosis of cone-rod dysfunction, including color vision described as severely abnormal and electroretinogram responses that showed absent cone a-wave but normal-to-subnormal rod function.

      CaseNotHPOs: HP:0000662 (Nyctalopia)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous genotyping was limited to homozygosity mapping of the sibling and his affected sister that identified a shared region of homozygosity on chromosome 13.

      CaseMethod1: Homozygosity mapping

      CaseMethod2: Sanger sequencing of CABP4

      CaseGenotypingMethod: Genotyping began with homozygosity mapping of the sibling and his affected sister that identified a shared region of homozygosity on chromosome 13, followed by Sanger sequencing of PCR products from the CABP4 gene.

      Variant: The individual harbors the NM_145200.5(CABP4):c.646C>T (p.Arg216Ter) variant in the homozygous state.

      ClinVar ID: 190959

      gnomAD: The variant is found in gnomAD version 4.1.1 at a frequency of 0.0001418 in the European (non-Finnish) population, with 0 homozygotes https://gnomad.broadinstitute.org/variant/chr11-67457677-C-T?dataset=gnomad_r4

      VariantEvidence: NM_145200.5(CABP4):c.646C>T (p.Arg216Ter) is a nonsense variant within exon 4 of 6 that is predicted to trigger nonsense-mediated decay.

      CaseAddInfo: The proband's family includes a similarly affected sister harboring the variant in the homozygous state, and unaffected parents who each carry the variant in the heterozygous state. Consanguinity has not been commented upon.

      CasePMIDs: N/A

    2. A null mutation in CABP4 causes Leber's congenital amaurosis-like phenotype

      PMID: 20157620

      Gene: CABP4

      HGNC: 1386

      Disease: cone-rod synaptic disorder, congenital nonprogressive

      MONDO: 0012490

      InheritancePattern: autosomal recessive

      Prevalence: The prevalence of the Åland eye disease or incomplete congenital stationary night blindness phenotype was estimated at 1 in 22,000 based on a Danish male cohort, with CABP4 variants specifically responsible for 1 out of 35 cases (PMID: 28002560).

      Penetrance: Penetrance appears to be 100% among the reported individuals harboring biallelic disease-causing CABP4 variants.

    1. Genome-wide homozygosity mapping, with a 250K SNP-array followed by a search for candidate genes, was performed. The patients underwent ophthalmic examination, including elaborate electroretinography. Results: In a Dutch sib pair, a shared 9-Mb homozygous region was found on 11q13.1-q13.5 that encompasses the CABP4 gene, previously implicated in autosomal recessive incomplete congenital stationary night blindness (CSNB2) in two small families. A novel homozygous p.Arg216X mutation in CABP4 was detected in the sib pair. Quantitative RT-PCR on RNA isolated from patient lymphoblast cells showed no nonsense-mediated degradation of mutant CABP4 mRNA. Clinically, patients presented with reduced visual acuity, photophobia, and abnormal color vision, but they did not experience night blindness. Electroretinograms showed electronegative mixed rod-cone responses and severely reduced cone responses, as in CSNB2. Isolated rod responses, however, were (sub)normal.

      Case#: Littink_2009_Family_Proband_II-1, male, onset in early childhood, age 12 years at time of report, family ancestry reported as Dutch

      CasePresentingHPOs: HP:0011463 (Childhood onset), HP:0000639 (Nystagmus), HP:0007663 (Reduced visual acuity), HP:0000613 (Photophobia), HP:0000551 (Color vision defect)

      CaseHPOFreeText: The proband and his sibling have a diagnosis of cone-rod dysfunction, including color vision described as severely abnormal and electroretinogram responses that showed absent cone a-wave but normal-to-subnormal rod function.

      CaseNotHPOs: HP:0000662 (Nyctalopia)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous genotyping was limited to homozygosity mapping of the sibling and his affected sister that identified a shared region of homozygosity on chromosome 13.

      CaseMethod1: Homozygosity mapping

      CaseMethod2: Sanger sequencing of CABP4

      CaseGenotypingMethod: Genotyping began with homozygosity mapping of the sibling and his affected sister that identified a shared region of homozygosity on chromosome 13, followed by Sanger sequencing of PCR products from the CABP4 gene.

      Variant: The individual harbors the NM_145200.5(CABP4):c.646C>T (p.Arg216Ter) variant in the homozygous state.

      ClinVar ID: 190959

      gnomAD: The variant is found in gnomAD version 4.1.1 at a frequency of 0.0001418 in the European (non-Finnish) population, with 0 homozygotes https://gnomad.broadinstitute.org/variant/chr11-67457677-C-T?dataset=gnomad_r4

      VariantEvidence: NM_145200.5(CABP4):c.646C>T (p.Arg216Ter) is a nonsense variant within exon 4 of 6 that is predicted to trigger nonsense-mediated decay.

      CaseAddInfo: The proband's family includes a similarly affected sister harboring the variant in the homozygous state, and unaffected parents who each carry the variant in the heterozygous state. Consanguinity has not been commented upon.

      CasePMIDs: N/A

    2. A novel homozygous nonsense mutation in CABP4 causes congenital cone-rod synaptic disorder

      PMID: 19074807

      Gene: CABP4

      HGNC: 1386

      Disease: cone-rod synaptic disorder, congenital nonprogressive

      MONDO: 0012490

      InheritancePattern: autosomal recessive

      Prevalence: The prevalence of the Åland eye disease or incomplete congenital stationary night blindness phenotype was estimated at 1 in 22,000 based on a Danish male cohort, with CABP4 variants specifically responsible for 1 out of 35 cases (PMID: 28002560).

      Penetrance: Penetrance appears to be 100% among the reported individuals harboring biallelic disease-causing CABP4 variants.

    1. Mutations in CABP4, the gene encoding the Ca2+-binding protein 4, cause autosomal recessive night blindness

      PMID: 16960802

      Gene: CABP4

      HGNC: 1386

      Disease: cone-rod synaptic disorder, congenital nonprogressive

      MONDO: 0012490

      InheritancePattern: autosomal recessive

      Prevalence: The prevalence of the Åland eye disease or incomplete congenital stationary night blindness phenotype was estimated at 1 in 22,000 based on a Danish male cohort, with CABP4 variants specifically responsible for 1 out of 35 cases (PMID: 28002560).

      Penetrance: Penetrance appears to be 100% among the reported individuals harboring biallelic disease-causing CABP4 variants.

    2. Ten of our patients with CSNB2 showed no mutation in CACNA1F. To identify the disease-causing mutations, we used a candidate-gene approach. CABP4, a member of the calcium-binding protein (CABP) family, is located in photoreceptor synaptic terminals and is directly associated with the C-terminal domain of the Cav1.4 alpha . Mice lacking either Cabp4 or Cav1.4 alpha display a CSNB2-like phenotype. Here, we report for the first time that mutations in CABP4 lead to autosomal recessive CSNB. Our studies revealed homozygous and compound heterozygous mutations in two families

      Case#: Zeitz_2006_Family_A_II-5, male, onset in early childhood, family ancestry reported as Swiss

      CasePresentingHPOs: HP:0011463 (Childhood onset), HP:0000639 (Nystagmus), HP:0007663 (Reduced visual acuity), HP:0000613 (Photophobia)

      CaseHPOFreeText: The proband and his sibling have diagnosis of congenital stationary night blindness, in the absence of family history of the disease. BCVA was 20/100 at age 15 years. Disease course was stationary for 30 years but later included a decrease in visual acuity and development of moderate photophobia.

      CaseNotHPOs: HP:0000662 (Nyctalopia)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous genotyping was limited to Sanger sequencing of PCR products from the CACNA1F gene. The authors also implied that similarly screening was performed all other known genes associated CSNB, which at the time included RHO, GNAT1, PDE6B, GRK1, SAG, NYX, and GRM6.

      CaseMethod1: Sanger sequencing of CABP4

      CaseMethod2: N/A

      CaseGenotypingMethod: Genotyping was limited to Sanger sequencing of PCR products from the CACNA1F and CABP4 genes, with possible sequencing of other known CSNB-associated genes RHO, GNAT1, PDE6B, GRK1, SAG, NYX, and GRM6.

      Variant: The individual harbors the NM_145200.3(CABP4):c.800_801delAG variant in the homozygous state.

      ClinVar ID: 1952

      gnomAD: The variant is found in gnomAD version 4.1.1 at a frequency of 0.00007043 in the European (non-Finnish) population, with 0 homozygotes https://gnomad.broadinstitute.org/variant/11-67226099-CAG-C?dataset=gnomad_r2_1

      VariantEvidence: NM_145200.3(CABP4):c.800_801delAG is a frameshift variant within exon 6 of 6 that is predicted not to trigger nonsense-mediated decay but rather to disrupt the C-terminal 9 amino acids (3%) of the protein product and to extend the remaining protein by 91 additional amino acids. Analysis of patient mRNA indicates that splicing occurs normally but that expression at the mRNA level is decreased by more than 50% relative to the unaffected family member control.

      CaseAddInfo: The proband's family is reportedly non-consanguineous, and includes a similarly affected brother who is also homozygous for the variant, as well as unaffected parents and 4 unaffected siblings who are heterozygous or lacking the variant (Figure 2A). Family history was negative for CSNB.

      CasePMIDs: N/A

    1. Essential role of Ca2+-binding protein 4, a Cav1.4 channel regulator, in photoreceptor synaptic function

      PMID: 15452577

      Gene: CABP4

      HGNC: 1386

      Disease: cone-rod synaptic disorder, congenital nonprogressive

      MONDO: 0012490

      InheritancePattern: autosomal recessive

      Prevalence: The prevalence of the Åland eye disease or incomplete congenital stationary night blindness phenotype was estimated at 1 in 22,000 based on a Danish male cohort, with CABP4 variants specifically responsible for 1 out of 35 cases (PMID: 28002560).

      Penetrance: Penetrance appears to be 100% among the reported individuals harboring biallelic disease-causing CABP4 variants.

    2. (f) Presynaptic localization of mouse CaBP4 (red) demonstrated by covisualization with a presynaptic protein (PSD95; green). Arrows indicate rod spherules and cone pedicles. (g) Colocalization of synaptic vesicle proteins SV2 and synaptophysin (green) with mouse CaBP4 (red).

      Biochemical evidence showing mouse CaBP4 (red) localization to the presynaptic region based on co-localization with the PSD95 marker (green).

    1. a novel CABP4 variation was identified in one family.

      Case#: Hove_2016_Proband_59, sex not reported, onset in early childhood, family ancestry reported as Danish

      CasePresentingHPOs: HP:0007750 (foveal hypoplasia)

      CaseHPOFreeText: The proband has a diagnosis of Aland Island eye disease and showed foveal hypoplasia in both eyes (supplement 2).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Previous genotyping may have been limited to Sanger sequencing of PCR products from the CACNA1F gene, or may have performed screening of other known genes associated with this phenotype.

      CaseMethod1: Sanger sequencing of CABP4

      CaseMethod2: N/A

      CaseGenotypingMethod: Genotyping was limited to Sanger sequencing of PCR products from the CACNA1F and CABP4 genes, with possible panel-based sequencing of other inherited retinal disease-associated genes.

      Variant: The individual harbors the NM_145200.5(CABP4):c.773A>T (p.Asn258Ile) variant in the homozygous state.

      ClinVar ID: 636004

      gnomAD: The variant is found in gnomAD version 4.1.1 at a frequency of 0.000001695 in the European (non-Finnish) population, with 0 homozygotes https://gnomad.broadinstitute.org/variant/chr11-67458492-A-T?dataset=gnomad_r4

      VariantEvidence: NM_145200.5(CABP4):c.773A>T (p.Asn258Ile) is a missense variant that does not have a characterized functional impact on CABP4..

      CaseAddInfo: No details are available regarding the potential for parental consanguinity.

      CasePMIDs: N/A

    1. Retinal findings in a patient of French ancestry with CABP4-related retinal disease

      PMID: 29525873

      Gene: CABP4

      HGNC: 1386

      Disease: cone-rod synaptic disorder, congenital nonprogressive

      MONDO: 0012490

      InheritancePattern: autosomal recessive

      Prevalence: The prevalence of the Åland eye disease or incomplete congenital stationary night blindness phenotype was estimated at 1 in 22,000 based on a Danish male cohort, with CABP4 variants specifically responsible for 1 out of 35 cases (PMID: 28002560).

      Penetrance: Penetrance appears to be 100% among the reported individuals harboring biallelic disease-causing CABP4 variants.