Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
The microcephaly ASPM gene is expressed in proliferating tissues and encodes for a mitotic spindle protein.
Human ASPM participates in spindle organisation, spindle orientation and cytokinesis.
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Human C-terminal-fragment perturbation supports spindle organization; fragment effects do not define native isoform function.
"ASPM C-terminal fragments expressed in transfected cells induce dominant-negative defects on spindle organisation and cytokinesis."
ASPM and citron kinase co-localize to the midbody ring during cytokinesis.
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ASPM and CITK co-associate in human HeLa lysates and embryonic neuroepithelium; this does not establish an isolated binary interface.
"coimmunoprecipitates with CITK in lysates prepared from HeLa cells and embryonic
neuroepithelium."
The microtubule-associated protein ASPM regulates spindle assembly and meiotic progression in mouse oocytes.
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The calmodulin association experiments used mouse material, rather than human oocytes.
"Lysates were prepared from MEFs and mouse MI-stage oocytes."
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The mouse experiments support calmodulin co-association.
"ASPM co-immunoprecipitated with calmodulin"
ASPM and CITK regulate spindle orientation by affecting the dynamics of astral microtubules.
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Spindle localization and rescue experiments connect ASPM with CITK.
"ASPM is required to recruit CITK
at the spindle, and CITK overexpression rescues ASPM phenotype."
Microtubule minus-end regulation at spindle poles by an ASPM-katanin complex.
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The purified ASPM preparation was the short mouse isoform with calmodulin, not purified human ASPM.
"we purified the short isoform of mouse ASPM in complex with calmodulin from overexpressing HEK293T cells"
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The separate endogenous human-cell experiment reports recruitment to newly produced microtubule minus ends.
"localized to freshly generated minus-ends"
Human microcephaly ASPM protein is a spindle pole-focusing factor that functions redundantly with CDK5RAP2.
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ASPM dependence is context-sensitive: ASPM deletion alone was tolerated in the reported human cells, with CDK5RAP2 depletion revealing a pole-focusing defect.
"Deletion of the ASPM gene
alone did not affect spindle morphology or mitotic progression."