Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
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
Automatic assignment of GO terms using logical inference, based on on inter-ontology links
Identification of a novel gene of the X,K-ATPase beta-subunit family that is predominantly expressed in skeletal and heart muscles.
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The 1999 discovery paper inferred an Na,K-ATPase isozyme from sequence alone.
"The data obtained indicate the existence of hitherto unknown X,K-ATPase (most probably Na,K-ATPase) isozymes in muscle cells."
Evolution of Na,K-ATPase beta m-subunit into a coregulator of transcription in placental mammals.
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Eutherian BetaM lost Na,K-ATPase function and moved to the nuclear membrane.
"In placental mammals beta m-proteins lost their ancestral functions, accumulate in nuclear membrane of perinatal myocytes, and associate with transcriptional coregulator Ski-interacting protein (SKIP)."
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BetaM regulates TGF-beta/Smad7 transcription via SKIP.
"Through interaction with SKIP, eutherian beta m acquired new functions as exemplified by regulation of TGF-beta-responsive reporters and by augmentation of mRNA levels of Smad7, an inhibitor of TGF-beta signaling."
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Human BetaM does not associate with Na,K-ATPase alpha-subunits.
"In contrast to human Na,K-ATPase β1(hβ1) used as a control (lanes 13–18), hβm was not coimmunoprecipitated with an α-antibody (lanes 7–12)."
A reference map of the human binary protein interactome.
Accumulation of beta (m), a structural member of X,K-ATPase beta-subunit family, in nuclear envelopes of perinatal myocytes.
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BetaM is in nuclei and nuclear membranes of neonatal muscle.
"Accordingly, beta(m) is detected by immunoblotting in purified nuclei and nuclear membranes from neonatal skeletal muscles."
Eutherian-Specific Functions of BetaM Acquired through Atp1b4 Gene Co-Option in the Regulation of MyoD Expression.
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BetaM binds the MyoD DRR and recruits BRG1.
"BetaM binds to the distal regulatory region (DRR) of MyoD, promotes epigenetic changes associated with activation of transcription, and recruits the SWI/SNF chromatin remodeling subunit, BRG1."
Evolutionary diversification of the BetaM interactome acquired through co-option of the ATP1B4 gene in placental mammals.
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BetaM binds LAP1, Syne1 and other partners.
"The inventory of identified BetaM interactors includes lamina-associated protein LAP-1, myocyte nuclear envelope protein Syne1, BetaM itself, heme oxidases HMOX1 and HMOX2; transcription factor LZIP/CREB3, ERGIC3, PHF3, reticulocalbin-3, and β-sarcoglycan."
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BetaM residues 72-98 mediate SKIP binding.
"Analysis of truncated forms of BetaM indicates that residues 72-98 adjacent to the membrane in nucleoplasmic domain are important for the interaction with SKIP."
Ablation of the Evolutionarily Acquired Functions of the Atp1b4 Gene Increases Metabolic Capacity and Reduces Obesity.
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Atp1b4-null mice are leaner, with higher energy expenditure.
"Male BetaM-deficient (Atp1b4-/Y) mice have remarkably lower body weight and adiposity than their wild-type littermates, despite higher food intake."
Reactome R-HSA-5252001: ATP1B4 binds SNW1
UniProt entry Q9UN42 (AT1B4_HUMAN)
Affinage mechanistic annotation for ATP1B4 (human)