# HISTORY
07 May 2016: Updated by: TOUCHUP-v1.18
16 Mar 2016: Updated by: TOUCHUP-v1.14
25 Mar 2016: Updated by: TOUCHUP-v1.15

# molecular_function

# cellular_component
20140207: Eumetazoa_PTN001032684 is found in mitochondrial outer membrane (GO:0005741) 
20140207: Chordata_PTN001032685 is found in endoplasmic reticulum (GO:0005783) 
20140207: Chordata_PTN001032685 is found in nuclear envelope (GO:0005635) 

# biological_process
20140207: Eumetazoa_PTN001032684 participates in mitochondrial outer membrane permeabilization (GO:0097345) 
20140207: Eumetazoa_PTN001032684 participates in regulation of programmed cell death (GO:0043067) 
20140207: Euteleostomi_PTN000796011 participates in positive regulation of programmed cell death (GO:0043068) 
20140207: Euteleostomi_PTN000795992 participates in negative regulation of programmed cell death (GO:0043069) 
20140207: Euteleostomi_PTN000795992 participates in defense response to virus (GO:0051607) 

# WARNINGS - THE FOLLOWING HAVE BEEN REMOVED FOR THE REASONS NOTED

# NOTES
- note that bnip3l is also known as nik and b5.
- Review: PMID:21126215
"B-cell leukemia/lymphoma 2 (BCL-2)/adenovirus E1B interacting protein 3 (BNIP3) and Nip-like protein X (NIX) are atypical BCL-2 homology domain 3-only proteins involved in cell death, autophagy, and programmed mitochondrial clearance. BNIP3 and NIX cause cell death by targeting mitochondria, directly through BCL-2-associated X protein- or BCL-2-antagonist/killer-dependent mechanisms, or indirectly through an effect on calcium stores in the endoplasmic reticulum. "
The proteins mediate a form of cell death that is caspase-independent, thus, non-apoptotic.... although PMID:2043645state that "According to cell type and stimuli, Bnip3 might induce cell death by apoptosis or autophagy. ", but in that paper they measure apoptosis by cytochrome c release and mitotracker, which I don't think is right.
The paper also mentions caspase-dependent cell death, without a reference.
CC
- Evidence for mitochondrial membrane localization across the entire trees; outer membrane is supported in the Chordata. Propagated to the entire tree because it seems unlikely that the protein is localized in different subcompartments.
- Nuclear localization: PMID: 10381623 "The C-terminal transmembrane domain is also required to localize B5 [BNIP3L] to nuclear envelope, endoplasmic reticulum and mitochondria, as does Nip3 and the Bcl-2 family members to these membranaceous structures. B5 has high sequence homology with Nip3 in the middle and C-terminal regions, but has unique sequence in the N-terminus" -> C terminus is not that conserved outside Chordata, so propagated 'nuclear membrane' to Chordata only.
- Propagated endiplasmic reticulim to Chordata since PMID:21126215 review states that "BNIP3 and NIX cause cell death (...)  indirectly through an effect on calcium stores in the endoplasmic reticulum. "
MF
- No MP propagated:
- Did not propagate lamin binding; paper states that "B5 [BNIP3L] interacted weakly with E1B19K and laminC, but not with laminA, although E1B19K interacts strongly with laminA and laminC."
- Did not propapate protease binding, because although there is evidence that BNIP3 family members interacts with caspases, they incude caspase-independent cell death (see PMID:15623420, PMID:16511341).
- Did not propagate GTPase binding (interactor is OPA1, see PMID:20436456), because the annotation is not informative.
BP
- Human BNIP3: PMID: 10891486  "BNIP3-mediated cell death is independent of Apaf-1, caspase activation, cytochrome c release, and nuclear translocation of apoptosis-inducing factor. However, cells transfected with BNIP3 exhibit early plasma membrane permeability, mitochondrial damage, extensive cytoplasmic vacuolation, and mitochondrial autophagy, yielding a morphotype that is typical of necrosis."
- Propagated "programmed cell death" to the entire family. BNIP3 and BNIP3L are not involved in apoptosis; they are involved in mitochondrial dependent programmed cell death.
- Propagated " mitochondrial outer membrane permeabilization (GO:0097345)" to the entire tree although it would be better to have a term describing the rols of  mitochondrial outer membrane permeabilization (GO:0097345) specifically in programmed cell death. Created a SF ticket for this: http://sourceforge.net/p/geneontology/ontology-requests/10648/
- Propagated "defense response to virus" to BNIP3L clade; a better term may have been "positive regulation of programmed cell death during defense response to virus".

# REFERENCE
Annotation inferences using phylogenetic trees
The goal of the GO Reference Genome Project, described in PMID 19578431, is to provide accurate, complete and consistent GO annotations for all genes in twelve model organism genomes. To this end, GO curators are annotating evolutionary trees from the PANTHER database with GO terms describing molecular function, biological process and cellular component. GO terms based on experimental data from the scientific literature are used to annotate ancestral genes in the phylogenetic tree by sequence similarity (ISS), and unannotated descendants of these ancestral genes are inferred to have inherited these same GO annotations by descent. The annotations are done using a tool called PAINT (Phylogenetic Annotation and INference Tool).