其他名稱： I kappa B alpha;I kappa B alpha;I(Kappa)B(alpha);I(Kappa)B(alpha);I-kappa-B-alpha; IkappaBalpha;IkB-alpha;IKBA;IKBA;IKBA_HUMAN;IKBalpha;MAD 3;MAD 3;MAD3;Major histocompatibility complex enhancer binding protein MAD3;Major histocompatibility complex enhancer binding protein MAD3;Major histocompatibility complex enhancer-binding protein MAD3;NF kappa B inhibitor alpha;NF-kappa-B inhibitor alpha;NFKBI;NFKBI;NFKBIA; NFKBIA;Nuclear factor of kappa light chain gene enhancer in B cells;Nuclear factor of kappa light chain gene enhancer in B cells;Nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor alpha;Nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor alpha.
實測條帶： about 40kd
信號通路： Chemokine;Apoptosis_Inhibition;Apoptosis_Mitochondrial;Apoptosis_Overview;Toll_Like;NOD-like receptor;RIG-I-like receptor;Cytosolic DNA-sensing pathway;T_Cell_Receptor;B_Cell_Antigen;Neurotrophin;Adipocytokine;Epithelial cell signaling in Helicobacter pylori infection;Pathways in cancer;Prostate cancer;Chronic myeloid leukemia;Small cell lung cancer;
功能： disease:Defects in NFKBIA are the cause of ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant (ADEDAID) [MIM:612132]. Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. ADEDAID is an ectodermal dysplasia associated with decreased production of pro-inflammatory cytokines and certain interferons, rendering patients susceptible to infection.,function:Inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL dimers in the cytoplasm through masking of their nuclear localization signals. On cellular stimulation by immune and proinflammatory responses, becomes phosphorylated promoting ubiquitination and degradation, enabling the dimeric RELA to tranlocate to the nucleus and activate transcription.,induction:Induced in adherent monocytes.,online information:NFKBIA mutation db,PTM:Phosphorylated; disables inhibition of NF-kappa-B DNA-binding activity.,PTM:Sumoylated; sumoylation requires the presence of the nuclear import signal.,PTM:Ubiquitinated; subsequent to stimulus-dependent phosphorylation on serines.,similarity:Belongs to the NF-kappa-B inhibitor family.,similarity:Contains 5 ANK repeats.,subcellular location:Shuttles between the nucleus and the cytoplasm by a nuclear localization signal (NLS) and a CRM1-dependent nuclear export.,subunit:Interacts with RELA; the interaction requires the nuclear import signal. Interacts with NKIRAS1 and NKIRAS2. Part of a 70-90 kDa complex at least consisting of CHUK, IKBKB, NFKBIA, RELA, IKBKAP and MAP3K14. Interacts with HBV protein X. Interacts with RWDD3; the interaction enhances sumoylation.,
相關產(chǎn)品： RS0001,RS0002,YM3028,YM3029
細胞定位： Cytoplasm. Nucleus. Shuttles between the nucleus and the cytoplasm by a nuclear localization signal (NLS) and a CRM1-dependent nuclear export. .
其他名稱： I kappa B alpha;I kappa B alpha;I(Kappa)B(alpha);I(Kappa)B(alpha);I-kappa-B-alpha; IkappaBalpha;IkB-alpha;IKBA;IKBA;IKBA_HUMAN;IKBalpha;MAD 3;MAD 3;MAD3;Major histocompatibility complex enhancer binding protein MAD3;Major histocompatibility complex enhancer binding protein MAD3;Major histocompatibility complex enhancer-binding protein MAD3;NF kappa B inhibitor alpha;NF-kappa-B inhibitor alpha;NFKBI;NFKBI;NFKBIA; NFKBIA;Nuclear factor of kappa light chain gene enhancer in B cells;Nuclear factor of kappa light chain gene enhancer in B cells;Nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor alpha;Nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor alpha.
實測條帶： about 40kd
信號通路： Chemokine;Apoptosis_Inhibition;Apoptosis_Mitochondrial;Apoptosis_Overview;Toll_Like;NOD-like receptor;RIG-I-like receptor;Cytosolic DNA-sensing pathway;T_Cell_Receptor;B_Cell_Antigen;Neurotrophin;Adipocytokine;Epithelial cell signaling in Helicobacter pylori infection;Pathways in cancer;Prostate cancer;Chronic myeloid leukemia;Small cell lung cancer;
功能： disease:Defects in NFKBIA are the cause of ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant (ADEDAID) [MIM:612132]. Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. ADEDAID is an ectodermal dysplasia associated with decreased production of pro-inflammatory cytokines and certain interferons, rendering patients susceptible to infection.,function:Inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL dimers in the cytoplasm through masking of their nuclear localization signals. On cellular stimulation by immune and proinflammatory responses, becomes phosphorylated promoting ubiquitination and degradation, enabling the dimeric RELA to tranlocate to the nucleus and activate transcription.,induction:Induced in adherent monocytes.,online information:NFKBIA mutation db,PTM:Phosphorylated; disables inhibition of NF-kappa-B DNA-binding activity.,PTM:Sumoylated; sumoylation requires the presence of the nuclear import signal.,PTM:Ubiquitinated; subsequent to stimulus-dependent phosphorylation on serines.,similarity:Belongs to the NF-kappa-B inhibitor family.,similarity:Contains 5 ANK repeats.,subcellular location:Shuttles between the nucleus and the cytoplasm by a nuclear localization signal (NLS) and a CRM1-dependent nuclear export.,subunit:Interacts with RELA; the interaction requires the nuclear import signal. Interacts with NKIRAS1 and NKIRAS2. Part of a 70-90 kDa complex at least consisting of CHUK, IKBKB, NFKBIA, RELA, IKBKAP and MAP3K14. Interacts with HBV protein X. Interacts with RWDD3; the interaction enhances sumoylation.,
相關產(chǎn)品： RS0001,RS0002,YM3028,YM3029
細胞定位： Cytoplasm. Nucleus. Shuttles between the nucleus and the cytoplasm by a nuclear localization signal (NLS) and a CRM1-dependent nuclear export. .
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