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SRCAP

Snf2 related CREBBP activator protein

The SRCAP gene encodes a protein integral to chromatin remodelling, a process vital for gene expression and proper cellular development. The SRCAP gene provides instructions for producing the Snf2 related CREBBP activator protein.

Chromosome 16p11.2 Autosomal dominant HGNC:16974 Tier C
SRCAP 16p11.2 p arm q arm 16

SRCAP is located on the short (p) arm of chromosome 16, at band 16p11.2. Arm ratio per GRCh38 - banding schematic.

Explore chromosome 16 in the library →

Overview

The SRCAP gene, also known as Snf2 related CREBBP activator protein, plays a significant role in gene regulation. It is involved in processes that control how DNA is packaged within the cell nucleus, which in turn affects gene expression. Understanding this gene's function helps explain normal human development and certain genetic conditions.

What the gene does

The protein encoded by the SRCAP gene forms part of a larger cellular complex that functions as a chromatin remodeller. This complex alters chromatin structure, which influences how accessible genes are for transcription. Research indicates that the SRCAP protein participates in activating the CREBBP gene. CREBBP produces CREB binding protein, which regulates cellular growth and division processes essential for typical human development. Through its chromatin-modifying activity, SRCAP influences gene expression across multiple biological processes.

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Chromosome location

The SRCAP gene is located on chromosome 16, specifically at position 16p11.2. This genomic address places it within the short arm of chromosome 16 and indicates its involvement in various cellular functions.

Protein structure

The SRCAP protein is quite large, consisting of 3230 amino acids. Disordered regions are present at amino acids 1-71, 253-547, 559-581, 1017-1045, 1058-1125, 1138-1166, 1320-1366, 1406-1425, 1629-1760, 1839-1893, 2214-2233, 2271-2298, 2327-2453, 2564-2583, and 2598-3081. Key functional domains include a HSA domain (amino acids 124-196), a Helicase ATP-binding domain (amino acids 630-795), and a Helicase C-terminal domain (amino acids 2044-2197). Within one of the larger disordered regions, there are two DNA-binding A.T hook domains, located at amino acids 2857-2869 and 2936-2948.

Domain map · 3,230 amino acids
HSA (124–196)Helicase ATP-binding (630–795)Helicase C-terminal (2044–2197)A.T hook 1 (2857–2869)A.T hook 2 (2936–2948)A.T hook 3 (3004–3016)HSA124–196Helicase ATP-binding630–795Helicase C-terminal2044–21971~1,6153,230
Domain - independent functional unit
Region - functional region
UniProt:Q6ZRS2Length:3,230 aa

Key variants

Variants within the SRCAP gene can lead to alterations in the protein's structure and function. These changes may impact its role in chromatin remodelling and gene expression. The clinical significance of any specific variant is determined through careful evaluation, considering its effect on protein activity and association with inherited conditions. Variants are often classified based on their predicted impact, ranging from benign to pathogenic.

2,388
Total variants catalogued in ClinVar
View all on ClinVar →
111 Pathogenic / Likely pathogenic 1,361 Uncertain significance 790 Benign / Likely benign 126 Conflicting or other

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.5633dup
Duplication
p.Pro1879fs Pathogenic/Likely pathogenic ★★☆☆ Developmental delay, hypotonia, musculoskeletal defects, and behavioral abnormalities
c.6985C>T
single nucleotide variant
p.Arg2329Ter Pathogenic/Likely pathogenic ★★☆☆ Floating-Harbor syndrome
c.7219C>T
single nucleotide variant
p.Gln2407Ter Pathogenic ★★☆☆ Inborn genetic diseases
c.7255C>T
single nucleotide variant
p.Gln2419Ter Pathogenic ★★☆☆ Floating-Harbor syndrome
c.7262dup
Duplication
p.Ser2422fs Pathogenic/Likely pathogenic ★★☆☆ not provided
c.7303C>T
single nucleotide variant
p.Arg2435Ter Pathogenic/Likely pathogenic ★★☆☆ Floating-Harbor syndrome
c.7330C>T
single nucleotide variant
p.Arg2444Ter Pathogenic ★★☆☆ Floating-Harbor syndrome
c.7376del
Deletion
p.Pro2459fs Pathogenic/Likely pathogenic ★★☆☆ Floating-Harbor syndrome
c.7382del
Deletion
p.Pro2461fs Pathogenic ★★☆☆ Floating-Harbor syndrome
c.7387del
Deletion
p.Ser2463fs Pathogenic ★★☆☆ not provided

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

Pathogenic variants in the SRCAP gene are associated with Floating-Harbour syndrome, an inherited condition. This syndrome is characterised by features including short stature, delayed bone age (slowing of bone mineralisation), delayed speech development, and distinctive facial features. Several SRCAP gene mutations have been identified in individuals with this syndrome. Conditions linked to SRCAP typically follow an autosomal dominant inheritance pattern, meaning that inheriting just one altered copy of the gene is sufficient to cause the condition.

Inheritance pattern

Conditions caused by pathogenic SRCAP variants typically follow autosomal dominant inheritance.

♀ Affected parent 1 altered copy ♂ Unaffected parent 2 typical copies Affected Unaffected Unaffected Affected Affected Carrier Unaffected Circles = females · Squares = males

Each child has a 50% chance of inheriting the pathogenic variant, regardless of sex.

UK clinical status

The SRCAP gene is reviewed by the UK National Health Service (NHS) Genomic Medicine Service. It is listed on several Green panels, indicating strong evidence for its association with specific conditions. These include the DDG2P panel, the Foetal anomalies panel (R21), the Intellectual disability panel (R29), the IUGR and IGF abnormalities panel, and the Monogenic short stature panel (R453).

Diet & lifestyle considerations

Currently, there are no specific lifestyle interventions known to prevent or treat conditions associated with SRCAP gene variants. General healthy lifestyle recommendations, such as a balanced diet and regular physical activity, are always advisable for overall well-being.

Supplement considerations

There is no conclusive scientific evidence to suggest that any specific supplements can prevent, treat, or mitigate the effects of conditions caused by SRCAP gene variants. Individuals should consult with a healthcare professional before considering any new supplements.

Frequently asked questions

What is the function of the SRCAP gene?

The SRCAP gene provides instructions for a protein that is a key component of a chromatin remodelling complex. This complex modifies DNA packaging, which is crucial for regulating gene expression and ensuring normal cell growth and development.

What condition is associated with the SRCAP gene?

Variants in the SRCAP gene are associated with Floating-Harbour syndrome. This condition typically presents with short stature, delayed bone development, speech delay, and specific facial characteristics.

How is Floating-Harbour syndrome inherited?

Floating-Harbour syndrome, when caused by SRCAP gene variants, follows an autosomal dominant inheritance pattern. This means that a person only needs to inherit one copy of the altered gene from a parent to develop the condition.

References

  1. Hood RL, Lines MA, Nikkel SM. Mutations in SRCAP, encoding SNF2-related CREBBP activator protein, cause Floating-Harbor syndrome. American journal of human genetics. 2012. PMID: 22265015
  2. Slupianek A, Yerrum S, Safadi FF. The chromatin remodeling factor SRCAP modulates expression of prostate specific antigen and cellular proliferation in prostate cancer cells. Journal of cellular physiology. 2010. PMID: 20432434
  3. Wong MM, Cox LK, Chrivia JC. The chromatin remodeling protein, SRCAP, is critical for deposition of the histone variant H2A.Z at promoters. The Journal of biological chemistry. 2007. PMID: 17617668
⚠ Draft content. This page has been flagged for manual clinical review and may contain gaps or inaccuracies. Speak with a qualified healthcare professional before acting on any information here.
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 19 July 2026. Content compiled from HGNC · MedlinePlus Genetics · ClinGen · Genomics England PanelApp · NHS National Genomic Test Directory · ClinVar · UniProt .