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PredicateObject
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http://www.biopax.org/relea...
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Influenza virus NS1A-binding protein homolog
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NS1BP_MOUSE
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Kelch family protein Nd1-L, ND1-L2, NS1-BP, NS1-binding protein homolog, Nd1-S
http://www.biopax.org/relea...
FUNCTION: Plays a role in cell division and in the dynamic organization of the actin skeleton as a stabilizer of actin filaments by association with F-actin through Kelch repeats. Protects cells from cell death induced by actin destabilization; Protects neurons from dendritic spines and actin filaments damage induced by the actin-destabilizing cytochalasin B when overexpressed. Play a role in protecting the heart from doxorubicin-induced cardiomyopathy. Activates Erk signaling pathway when overexpressed in cultured cell lines. SUBUNIT: Homodimer; through the BTB domain. Interacts with AHR/Aryl hydrocarbon receptor (By similarity). SUBCELLULAR LOCATION: Isoform 1: Cytoplasm. Cytoplasm, cytoskeleton. Note=Associated with actin filaments. SUBCELLULAR LOCATION: Isoform 2: Nucleus. ALTERNATIVE PRODUCTS: Event=Alternative splicing; Named isoforms=4; Name=1; Synonyms=Nd1-L; IsoId=Q920Q8-1; Sequence=Displayed; Name=2; Synonyms=Nd1-S; IsoId=Q920Q8-2; Sequence=VSP_024812, VSP_024813; Name=3; Synonyms=Nd1-L2; IsoId=Q920Q8-3; Sequence=VSP_024811; Name=4; IsoId=Q920Q8-4; Sequence=VSP_024810; Note=No experimental confirmation available; TISSUE SPECIFICITY: Ubiquitous expression. In the heart, the highest expression is detected in the ventricles and the lowest in the atria. Expressed in dendrites and spines in neurons. DEVELOPMENTAL STAGE: Barely detected in the heart at E15.5, but clearly expressed in newborn heart with increased amount up to 8 weeks of age. INDUCTION: Decreased expression in various organs and cultured cell lines by doxorubicin treatment which may reduces mRNA stability. DOMAIN: When the BTB domain is lacking, AHR signaling induction promoted by IVNS1ABP is massively increased; Thus, the BTB domain inhibits AHR signaling induced by IVNS1ABP (By similarity). DISRUPTION PHENOTYPE: Mice develop normally with no gross abnormalities. However, they display marked sensitivity to doxorubicin cardiotoxicity with increased number of cardiomyocytes apoptosis. Analysis of hearts from knockout mice reveal vacuolization and edema of cardiomaycytes. MISCELLANEOUS: Transgenic mice overexpressing Ivns1abp develop normally with no gross abnormalities up to 7-month old. However, they display a marked resistance to the cardiotoxic effect of doxorubicin which is an anti-neoplastic agent known to affect actin skeleton and an effective drug for cancer therapy with cardiotoxicity as side effect. Overexpression of Ivns1abp in the heart protect cardiomyocytes from apoptosis and improved survival rate after doxorubicin injection. MISCELLANEOUS: Disorganized actin sleleton is observed in cells transfected with isoform 2 (Nd1-S), which lacks the six kelch repeats. SIMILARITY: Contains 1 BACK (BTB/Kelch associated) domain. SIMILARITY: Contains 1 BTB (POZ) domain. SIMILARITY: Contains 6 Kelch repeats. SEQUENCE CAUTION: Sequence=BAC98039.1; Type=Erroneous initiation; GENE SYNONYMS: Kiaa0850 Nd1 Nd1L Nd1S Ns1 Ns1bp. COPYRIGHT: Protein annotation is derived from the UniProt Consortium (http://www.uniprot.org/). Distributed under the Creative Commons Attribution-NoDerivs License.
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