protein
Annexin A11
Gene
ANXA11
Organism
Homo sapiens(9606)
Length
505 aa
Mass
54,390 Da
Annexin A11 (ANXA11) is a calcium-binding protein of 505 amino acids that plays a role in cytokinesis, specifically required for midbody formation and completion of the terminal phase of cell division (UniProt: P50995). It binds calcyclin in a calcium-dependent manner and is expressed in human tissues.
Beyond its cell-cycle function, ANXA11 has been associated with neurodegenerative diseases. Mutations in ANXA11 cause amyotrophic lateral sclerosis 23 (ALS23), an autosomal dominant motor neuron disease featuring ubiquitin-positive inclusions and pathologic aggregates (UniProt: P50995). The protein is also implicated in inclusion body myopathy with brain white matter abnormalities (IBMWMA), an adult-onset disorder characterized by muscle weakness, cognitive decline, and cytoplasmic protein aggregates.
In Alzheimer's disease, ANXA11 is significantly upregulated in post-mortem AD brain tissue compared to age-matched controls (mean log2 fold-change = 0.17; Chaparral AD proteomics). This elevation was detected across subcellular fractions in a TMT-labeled proteomic study, suggesting involvement in AD-related pathological processes, potentially linking the protein's aggregation-related functions to amyloid and tau pathology.
Generated from the curated entity record below. May contain errors — verify against source links.
Proteomics Evidence · AD
↑ Up in ADP3
not detected
P2
not detected
S2
not detected
S3
+0.171
Mean log₂FC across detected fractions: +0.1712 (1 of 4 fractions detected)
Human post-mortem AD brain vs age-matched controls, TMT-labeled, 4 subcellular fractions (P2, P3, S2, S3), DDA proteomics.
Related Publications
Browse all →Tau molecular diversity contributes to clinical heterogeneity in Alzheimer's disease.
Dujardin Simon et al.Nature medicine2020PMID 32572268Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer's Disease Progression.
Bai Bing et al.Neuron2020PMID 31926610A Multi-network Approach Identifies Protein-Specific Co-expression in Asymptomatic and Symptomatic Alzheimer's Disease.
Seyfried Nicholas T et al.Cell systems2017PMID 27989508Large-scale deep multi-layer analysis of Alzheimer's disease brain reveals strong proteomic disease-related changes not observed at the RNA level.
Johnson Erik C B et al.Nature neuroscience2022PMID 35115731Organization and regulation of gene transcription.
Cramer PatrickNature2019PMID 31462772
Function
Binds specifically to calcyclin in a calcium-dependent manner (By similarity). Required for midbody formation and completion of the terminal phase of cytokinesis
Disease associations
Amyotrophic lateral sclerosis 23ALS23
A form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. ALS23 is an autosomal dominant form with incomplete penetrance.
Inclusion body myopathy and brain white matter abnormalitiesIBMWMA
An autosomal dominant, adult-onset disorder characterized predominantly by proximal limb girdle muscle weakness affecting the lower and upper limbs and resulting in gait difficulties and scapular winging. Additional features may include dysarthria, dysphagia, low back pain, and hyporeflexia. Muscle biopsy shows fiber type variation, internal nuclei, rimmed vacuoles, and cytoplasmic protein aggregates or inclusions. Cognitive impairment or frontotemporal dementia occurs in some patients.
Sources
Last updated 5/8/2026, 6:33:09 AM