Autophagy protein 5 (APG5-like) (Apoptosis-specific protein)
1_MTDDK 6_ DVLRD 11_ VWFGR 16_ IPTCF 21_ TLYQD 26_ EITER 31_ EAEPY 36_ YLLLP 41_ RVSYL 46_ TLVTD 51_ KVKKH 56_ FQKVM 61_ RQEDI 66_ SEIWF 71_ EYEGT 76_ PLKWH 81_ YPIGL 86_ LFDLL 91_ ASSSA 96_ LPWNI 101_ TVHFK 106_ SFPEK 111_ DLLHC 116_ PSKDA 121_ IEAHF 126_ MSCMK 131_ EADAL 136_ KHKSQ 141_ VINEM 146_ QKKDH 151_ KQLWM 156_ GLQND 161_ RFDQF 166_ WAINR 171_ KLMEY 176_ PAEEN 181_ GFRYI 186_ PFRIY 191_ QTTTE 196_ RPFIQ 201_ KLFRP 206_ VAADG 211_ QLHTL 216_ GDLLK 221_ EVCPS 226_ AIDPE 231_ DGEKK 236_ NQVMI 241_ HGIEP 246_ MLETP 251_ LQWLS 256_ EHLSY 261_ PDNFL 266_HISII
1: Involved in autophagic vesicle formation. Conjugation with ATG12, through a ubiquitin-like conjugating system involving ATG7 as an E1-like activating enzyme and ATG10 as an E2-like conjugating enzyme, is essential for its function. The ATG12-ATG5 conjugate acts as an E3-like enzyme which is required for lipidation of ATG8 family proteins and their association to the vesicle membranes. Involved in mitochondrial quality control after oxidative damage, and in subsequent cellular longevity. Plays a critical role in multiple aspects of lymphocyte development and is essential for both B and T lymphocyte survival and proliferation. Required for optimal processing and presentation of antigens for MHC II. Involved in the maintenance of axon morphology and membrane structures, as well as in normal adipocyte differentiation. Promotes primary ciliogenesis through removal of OFD1 from centriolar satellites and degradation of IFT20 via the autophagic pathway. As part of the ATG8 conjugation system with ATG12 and ATG16L1, required for recruitment of LRRK2 to stressed lysosomes and induction of LRRK2 kinase activity in response to lysosomal stress (By similarity)
2: May play an important role in the apoptotic process, possibly within the modified cytoskeleton. Its expression is a relatively late event in the apoptotic process, occurring downstream of caspase activity. Plays a crucial role in IFN-gamma-induced autophagic cell death by interacting with FADD
3: (Microbial infection) May act as a proviral factor. In association with ATG12, negatively regulates the innate antiviral immune response by impairing the type I IFN production pathway upon vesicular stomatitis virus (VSV) infection (PubMed:17709747). Required for the translation of incoming hepatitis C virus (HCV) RNA and, thereby, for initiation of HCV replication, but not required once infection is established (PubMed:19666601)