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ARL2BP

ARF like GTPase 2 binding protein

Chromosome 16q13 Autosomal recessive HGNC:17146 Tier C
Why it's called ARL2BP
ADP-Ribosylation Factor-Like GTPase 2 Binding Protein
Named for its binding to ARL2, a small GTPase in the ARF family.
ARL2BP 16q13 p arm q arm 16

ARL2BP is located on the long (q) arm of chromosome 16, at band 16q13. Arm ratio per GRCh38 - banding schematic.

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Overview

ARL2BP (ARF like GTPase 2 binding protein) is located on chromosome 16 and encodes a relatively small protein of 163 amino acids. This protein functions primarily as a binding partner for ARL2, a regulatory GTPase involved in microtubule dynamics and ciliary assembly. Cilia are hair-like projections on cell surfaces that serve essential roles in sensory perception, including vision, and in establishing the proper left-right arrangement of internal organs during development.

Pathogenic variants in ARL2BP follow an autosomal recessive inheritance pattern, meaning that affected individuals typically inherit altered copies from both parents. The gene has clinical relevance in ophthalmology, particularly for retinal disorders, and is included on several NHS clinical panels for diagnostic evaluation of conditions affecting the eye and organ positioning.

What the gene does

The ARL2BP protein serves as a binding partner and regulator of ARL2, a small GTPase that coordinates microtubule organisation and ciliary assembly. Through its interaction with ARL2, ARL2BP influences the proper formation and function of primary cilia, which are sensory organelles projecting from most mammalian cells. In photoreceptor cells of the retina, cilia are essential for the structural integrity of the outer segment, where light detection occurs.

This protein participates in intracellular trafficking pathways that deliver proteins and membranes to the cilium. The ARL2-ARL2BP complex appears to regulate tubulin cofactor interactions, which are critical for maintaining the microtubule cytoskeleton that forms the ciliary axoneme. Disruption of these processes can impair ciliary function, leading to defects in sensory perception and developmental signalling pathways that depend on ciliary activity. The protein's role extends beyond the retina, as cilia are also required for establishing left-right asymmetry during embryonic development.

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Chromosome location

ARL2BP is located on the long arm of chromosome 16 at position 16q13. This chromosomal region contains several genes involved in developmental processes and sensory function. The gene's compact coding sequence reflects the relatively small size of the encoded protein. Specific details regarding the total number of exons and transcript variants have not been extensively characterised in publicly available databases.

Protein structure

Domain architecture has not been experimentally characterised in detail for this protein. The ARL2BP protein comprises 163 amino acids and lacks well-annotated functional domains in current structural databases. Its molecular function is understood primarily through its binding interaction with ARL2 GTPase, though the precise regions mediating this interaction have not been mapped to specific structured domains. The protein's compact size suggests it may function as a relatively simple adaptor or regulatory module.

Key variants

Pathogenic variants in ARL2BP are inherited in an autosomal recessive manner, requiring changes in both gene copies to cause disease. The variant spectrum includes loss-of-function changes such as nonsense mutations and frameshift deletions that disrupt protein production. Missense variants affecting critical residues involved in ARL2 binding have also been reported. The clinical severity and specific manifestations can vary depending on the nature of the variants present, though retinal involvement is a common feature.

The table below shows the top 10 pathogenic or likely-pathogenic variants currently classified in ClinVar for ARL2BP.
View all on ClinVar →

Sample of pathogenic variants

10 pathogenic / likely-pathogenic variants from ClinVar, ranked by review status (expert-panel-reviewed first). This is a sample; recurrent founder variants in a specific population may not appear here - see the full ClinVar listing via the link above.

Variant (HGVS) Protein change Classification Evidence Associated condition
c.207+1G>A
single nucleotide variant
- Pathogenic ★★☆☆ ARL2BP-related disorder
c.139_143dup
Duplication
p.Tyr48Ter Pathogenic ★☆☆☆ not provided
c.191del
Deletion
p.Pro64fs Pathogenic ★☆☆☆ not provided
c.207C>A
single nucleotide variant
p.Tyr69Ter Pathogenic ★☆☆☆ not provided
c.235G>T
single nucleotide variant
p.Glu79Ter Pathogenic ★☆☆☆ not provided
c.33_36del
Deletion
p.Phe13fs Pathogenic ★☆☆☆ Retinitis pigmentosa
c.37_38del
Deletion
p.Phe13fs Pathogenic ★☆☆☆ Retinal dystrophy
c.97_98dup
Duplication
p.Met33fs Pathogenic ★☆☆☆ not provided
c.22_23del
Microsatellite
p.Ser8fs Pathogenic - Retinitis pigmentosa with or without situs inversus
c.294-1G>C
single nucleotide variant
- Pathogenic - Retinitis pigmentosa with or without situs inversus

Evidence stars indicate ClinVar review status. Individual variant interpretation should always be performed by a qualified clinical laboratory - many variants remain classified as Variants of Uncertain Significance (VUS) pending more research.

Associated conditions

Variants in ARL2BP are associated with autosomal recessive conditions primarily affecting the retina and, in some cases, organ positioning. Retinal dystrophies caused by ARL2BP variants typically involve progressive degeneration of photoreceptor cells, leading to vision impairment. Some affected individuals may present with laterality defects, where internal organs develop abnormal left-right positioning, reflecting the gene's role in ciliary signalling during embryonic development. The phenotypic spectrum ranges from isolated retinal disease to syndromic presentations involving multiple organ systems.

No disease links recorded for this gene in our reference set.

Inheritance pattern

Conditions caused by pathogenic ARL2BP variants typically follow autosomal recessive inheritance.

Carrier parent 1 altered copy Carrier parent 1 altered copy Affected Carrier Carrier Unaffected Affected Carrier Unaffected Circles = females · Squares = males

When both parents are carriers, each child has a 25% chance of being affected, 50% of being a carrier, and 25% of being unaffected.

Carrier frequency by population How common is heterozygous ARL2BP carrier status across ancestry groups?

UK clinical status

ARL2BP is included on three NHS Genomic Medicine Service panels as a green gene, indicating strong evidence for its clinical validity. The gene appears on the Retinal disorders panel (R32), reflecting its established role in inherited retinal disease. It is also listed on the Fetal anomalies panel (R21) and the Laterality disorders and isomerism panel (R139), acknowledging its association with developmental abnormalities affecting organ positioning. This panel membership supports the use of ARL2BP testing in UK clinical diagnostic pathways for patients presenting with retinal degeneration or laterality defects.

Frequently asked questions

What inheritance pattern does ARL2BP follow?

ARL2BP variants are inherited in an autosomal recessive pattern, meaning an individual must inherit a pathogenic variant from both parents to develop an associated condition. Carriers with one variant typically do not show symptoms.

How does ARL2BP relate to retinal health?

The ARL2BP protein supports ciliary function in photoreceptor cells, which are essential for light detection in the retina. Disruption of this function can lead to progressive retinal degeneration and vision loss.

Why is ARL2BP included on laterality disorder panels?

Primary cilia, which depend on ARL2BP function, play a crucial role in establishing left-right body asymmetry during embryonic development. Variants affecting ciliary function can therefore result in abnormal organ positioning.

Educational content. This page is not medical or genetic advice, is not individually reviewed by a clinician for each reader, and should not replace a consultation with a qualified healthcare professional or genetic counsellor. If you are considering genetic testing or acting on a test result, book a consultation.
Data sources Last updated 17 April 2026. Content compiled from HGNC · MedlinePlus Genetics · ClinGen · Genomics England PanelApp · NHS National Genomic Test Directory · ClinVar · UniProt · AlphaFold .