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Symbol ATG5 contributors: mct/ - updated : 24-10-2018
HGNC name ATG5 autophagy related 5 homolog (S. cerevisiae)
HGNC id 589
Corresponding disease
SCAR25 spinocerebellar ataxia, autosomal recessive 25
Location 6q21      Physical location : 106.632.353 - 106.773.695
Synonym name
  • apoptosis specific protein
  • APG5 autophagy 5-like (S. cerevisiae)
  • autophagy protein 5
  • APG5-like
  • Synonym symbol(s) ASP, APG5, APG5L, hAPG5, SCAR25, APG5-LIKE
    TYPE functioning gene
    STRUCTURE 141.34 kb     8 Exon(s)
    MAPPING cloned Y linked N status provisional
    Map cen - D6S434 - D6S283 - D6S1692 - ATG5 - D6S278 - RPL3 - D6S1635 - D6S1594 - D6S302 - qter
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    8 - 3244 32.3 275 - 1999 10702672
    5 - 2890 - 91 - 1999 10702672
    7 - 3132 - 197 - 1999 10702672
    8 - 3256 - 213 - 1999 10702672
    8 - 3125 - 275 - 1999 10702672
    Type ubiquitous
       expressed in (based on citations)
    cell lineage
    cell lines mammalian cell line
    at STAGE
  • a high number of acidic residues
  • a potential glycosylation site
  • potential casein kinase II, protein kinase C and tyrosine kinase sites
  • conjugated Other
    interspecies homolog to yeast S .cerevisiae Apg5p
    homolog to murine Apg5l
    homolog to Drosophila CG1643
  • ATG5 family
  • CATEGORY regulatory
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,organelle,endoplasmic reticulum
    text colocalizes with non-muscle actin
    basic FUNCTION
  • involved in autophagy
  • ATG12-ATG5 conjugate has a novel E3-like activity for protein lipidation in autophagy
  • ATG5-ATG12 conjugate, a key regulator of the autophagic process, plays an important role in innate antiviral immune responses
  • important for B cell survival during development and is differentially required at discrete stages of development in distinct, but closely related, cell lineages
  • involved in normal adipocyte differentiation, suggesting an important role of autophagy in adipogenesis
  • MAP1LC3B and ATG5 are not required for initiation of autophagy but mediate phagophore expansion and autophagosome formation
  • required in antigen presentation by dendritic cells
  • with ATG12, ATG2B, ATG9B, are autophagy-related genes, having mononucleotide repeats with seven or more nucleotides
  • MAP1LC3B, ATG5 and ATG12 are involved in mitochondrial quality control after oxidative damage, and to cellular longevity
  • regulates the formation of MYD88 condensed structures through association with MYD88 and eventually exerts a modulatory effect on MYD88-dependent signaling
  • dual role for ATG5 in response to drug-induced DNA damage, where it acts in two signalling pathways in two distinct cellular compartments, the cytosol and the nucleus
  • has a crucial role in cortical neurogenesis during early embryonic brain development, which may contribute to the understanding of neurodevelopmental disorders caused by autophagy dysregulation
  • role of ATG5 in the dynamic regulation of ligation-induced cellular senescence and apoptosis
  • ATG5-mediated autophagy in proximal epithelial cells is a critical host-defense mechanism that prevents renal fibrosis by blocking G2/M arrest
  • important role of ATG5 and autophagy in maintaining the function of neutrophil extracellular traps (NETs) formation in response to infection and in regulating neutrophil death
  • chronic morphine exposure caused ATG5 and ATG7-dependent and dopaminergic neuron-specific autophagy resulting in decreased neuron dendritic spines and the onset of addictive behaviors
  • ATG5- and ATG7-dependent autophagy of dopaminergic neurons contributed to cellular and behavioral responses to morphine
  • CELLULAR PROCESS cell life, cell death/apoptosis
    text highly expressed in apoptotic cells
    involved in ATG5/ATG7-dependent conventional pathway for macroautophagy
    a component
  • conjugation of the K-130 to the G-140 of APG12 is a covalent modification that is essential for autophagy
  • is a key component of an E3-like ATG12-ATG5-ATG16L1 protein complex that catalyzes conjugation of the MAP1LC3 protein to lipids, thus controlling autophagic vesicle formation and expansion
    small molecule
  • binding to ATG12
  • ATG10 interacts with ATG7 to receive an ubiquitin-like protein ATG12, recognizes both ATG12 and ATG5 directly and catalyzes their conjugation reaction
  • direct interaction between ATG5 and ATG16L1 is crucial to the performance of their roles in autophagy
  • single known conjugation target of ATG12
  • concerted interactions among TECPR1, ATG12-ATG5, and PtdIns(3)P provide the fusion specificity between autophagosomes and lysosomes and the assembly of this complex initiates the autophagosome maturation process
  • autophagic E2 enzymes, ATG10, interacts with ATG7 to receive ATG12, a ubiquitin-like molecule, and is also involved in the ATG12-ATG5 conjugation reaction
  • ATG5, a key regulatory protein of autophagy, inhibits the formation of MYD88 condensed structures
  • ELAVL4 is an inducer of ATG5 expression and hence a critical regulator of autophagosome formation in pancreatic beta cells
  • during process of induced autophagy, the ATG12-ATG5 conjugate requires 2 different binding partners, ATG16L1 for autophagosome elongation and TECPR1 for lysosomal fusion
  • TECPR1 and ATG16L1 share the same binding site on ATG5 (swapping of interaction partners with ATG5 for autophagosome maturation)
  • MUL1, a mitochondria-localized E3 ligase, regulates selenite-induced mitophagy in an ATG5 and ULK1-dependent manner
  • RACK1 is a novel ATG5 interactor and an autophagy protein
  • beneficial role of hypothalamic ATF4/ATG5 axis in the regulation of energy expenditure, obesity, and obesity-related metabolic disorders
  • mechanistically, BSN was found to interact with ATG5, an E3-like ligase essential for autophagy, and to inhibit the induction of autophagy in heterologous cells
  • cell & other
  • binding to isolation membrane
    induced by apoptotic stimuli
    corresponding disease(s) SCAR25
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional   deletion    
    led to increased mitochondrial mass in peripheral T cells
    constitutional     --over  
    in autoimmune demyelination and multiple sclerosis
    tumoral somatic mutation      
    in gastric and colorectal cancers with microsatellite instability
    Susceptibility to development of hepatocellular carcinoma (HCC)
    Variant & Polymorphism other
  • ATG5 rs17067724 significantly associated with HCC risk
  • Candidate gene
    Therapy target
    ATF4/ATG5 axis in the hypothalamus may be a new potential therapeutic target for treating obesity and obesity-related metabolic diseases
  • All Atg5-null mice died within 1 day of delivery, the survival time of starved Atg5-deficient neonates (approximately 12 hours) was much shorter than that of wildtype mice (approximately 21 hours). Atg5-deficient neonates exhibited reduced amino acid concentrations in plasma and tissues and displayed signs of energy depletion. Neonates adapt to immediate post-birth starvation by inducing autophagy
  • mice deficient for Atg5 or Atg7 specifically in the dopaminergic neurons were less sensitive to developing a morphine reward response, behavioral sensitization, analgesic tolerance and physical dependence compared to wild-type mice
  • Atg5-deficient mice displayed abnormal Tbx2 expression and defects in valve development and chamber septation