TCDB is operated by the Saier Lab Bioinformatics Group
TCIDNameDomainKingdom/PhylumProtein(s)
8.A.122.1.1









Neurensin-1, NRSN1, Neuro-p24, vesicular membrane protein of 24kDa, VMP-p24 of 195 aas and 2 TMSs.  May play a role in neural organelle transport, and in transduction of nerve signals or in nerve growth. May also play a role in neurite extension (Nagata et al. 2006Nagata et al. 2006).

Eukaryota
Metazoa
Neuensin-1 of Homo sapiens
8.A.122.1.2









Neurensin-2 (NRSN2) of 204 aas and 2 TMSs.  Both Neurensin-1, and -2 are localized to small vesicles in neural cells (Nakanishi et al. 2006). NRSN2 promotes lung and ovarian cancer as well as osteosarcoma cell proliferation and growth (Zhang et al. 2015; Keremu et al. 2017; Nakanishi et al. 2006). NRSN2 promotes lung and ovarian cancer as well as osteosarcoma cell proliferation and growth (Zhang et al. 2015; Keremu et al. 2017; Zhang et al. 2015; Keremu et al. 2017; Keremu et al. 2017; Tang et al. 2017Tang et al. 2017).

Eukaryota
Metazoa
Neurensin-2 of Homo sapiens
8.A.122.1.3









Neurensin-1 of 195 aas and 2 TMSs.

Eukaryota
Metazoa
Neurensin-1 of Jaculus jaculus (lesser Egyptian jerboa)
8.A.122.2.1









TMEM74 (ATG16L1) of 305 aas and 2 TMSs. An autosomal lysosomal protein that regulates autophagy (Yu et al. 2008). A coding polymorphism of human ATG16L1 (T300A) increases the risk of Crohn's disease and enhance susceptibility of ATG16L1 to caspase cleavage. T300A also alters the ability of the C-terminal WD40-repeat domain of ATG16L1 to interact with an amino acid motif that recognizes this region. Such alteration impairs the unconventional autophagic activity of TMEM59, a transmembrane protein that contains the WD40 domain-binding motif, and disrupts its normal intracellular trafficking and its ability to engage ATG16L1 in response to bacterial infection. TMEM59-induced autophagy is blunted in cells expressing the fragments generated by caspase processing of the ATG16L1-T300A risk allele, whereas canonical autophagy remains unaffected. Thus, the T300A polymorphism alters the function of motif-containing molecules that engage ATG16L1 through the WD40 domain, either by influencing this interaction under non-stressful conditions or by inhibiting their downstream autophagic signalling after caspase-mediated cleavage (Yu et al. 2008). A coding polymorphism of human ATG16L1 (T300A) increases the risk of Crohn's disease and enhance susceptibility of ATG16L1 to caspase cleavage. T300A also alters the ability of the C-terminal WD40-repeat domain of ATG16L1 to interact with an amino acid motif that recognizes this region. Such alteration impairs the unconventional autophagic activity of TMEM59, a transmembrane protein that contains the WD40 domain-binding motif, and disrupts its normal intracellular trafficking and its ability to engage ATG16L1 in response to bacterial infection. TMEM59-induced autophagy is blunted in cells expressing the fragments generated by caspase processing of the ATG16L1-T300A risk allele, whereas canonical autophagy remains unaffected. Thus, the T300A polymorphism alters the function of motif-containing molecules that engage ATG16L1 through the WD40 domain, either by influencing this interaction under non-stressful conditions or by inhibiting their downstream autophagic signalling after caspase-mediated cleavage (Boada-Romero et al. 2016).

Eukaryota
Metazoa
TMEM74 of Homo sapiens
8.A.122.2.2









Transmembrane protein 74B, TMEM74B of 160 aas and 2 TMSs.

Eukaryota
Metazoa
TMEM74B of Haliaeetus leucocephalus (Bald eagle)
8.A.122.2.3









Uncharacterized protein of 144 aas and 2 TMSs.

Eukaryota
Metazoa
UP of Crassostrea virginica (eastern oyster)