Description: Innovita COVID-19 IgG/IgM Rapid Test

Description: COVID-19 IgG/IgM Rapid Test (Serum/Plasma/Whole Blood) is a qualitative membrane-based immunoassay for the detection of COVID-19 antibodies in serum, plasma, or whole blood. This test consists of two test lines, an IgG line and an IgM line, which is pre-coated with two mouse anti-human monoclonal antibodies separately. During testing, the sample reacts with COVID-19 antigen-coated on conjugated pad. As the complex continues to travel up the strip, the anti-COVID-19 IgM antibodies are bound on the IgM line, and the anti-COVID-19 IgG antibodies are bound on the IgG line. The control(C)line appears when sample has flowed through the strip. The presence of anti-COVID-19 IgM and/or IgG will be indicated by a visible test line in the IgM and IgG region. To serve as a procedural control, the control line should always appear if the test procedure is performed properly and the reagents are working as intended.

Description: Contents: (1) 10 Tests/Kit   (cassette,disposable dropper,desiccant) (2) 10 Assay buffer tubes (3) 10 Sterile swabs (4) 1 Instruction manual

Description: Serine/threonine-protein kinase component of the chromosomal passenger complex (CPC), a complex that acts as a key regulator of mitosis. The CPC complex has essential functions at the centromere in ensuring correct chromosome alignment and segregation and is required for chromatin-induced microtubule stabilization and spindle assembly. Involved in the bipolar attachment of spindle microtubules to kinetochores and is a key regulator for the onset of cytokinesis during mitosis. Required for central/midzone spindle assembly and cleavage furrow formation. Key component of the cytokinesis checkpoint, a process required to delay abscission to prevent both premature resolution of intercellular chromosome bridges and accumulation of DNA damage: phosphorylates CHMP4C, leading to retain abscission-competent VPS4 (VPS4A and/or VPS4B) at the midbody ring until abscission checkpoint signaling is terminated at late cytokinesis. AURKB phosphorylates the CPC complex subunits BIRC5/survivin, CDCA8/borealin and INCENP. Phosphorylation of INCENP leads to increased AURKB activity. Other known AURKB substrates involved in centromeric functions and mitosis are CENPA, DES/desmin, GPAF, KIF2C, NSUN2, RACGAP1, SEPT1, VIM/vimentin, GSG2/Haspin, and histone H3. A positive feedback loop involving GSG2 and AURKB contributes to localization of CPC to centromeres. Phosphorylation of VIM controls vimentin filament segregation in cytokinetic process, whereas histone H3 is phosphorylated at 'Ser-10' and 'Ser-28' during mitosis (H3S10ph and H3S28ph, respectively). A positive feedback between GSG2 and AURKB contributes to CPC localization. AURKB is also required for kinetochore localization of BUB1 and SGOL1. Phosphorylation of p53/TP53 negatively regulates its transcriptional activity. Key regulator of active promoters in resting B- and T-lymphocytes: acts by mediating phosphorylation of H3S28ph at active promoters in resting B-cells, inhibiting RNF2/RING1B-mediated ubiquitination of histone H2A and enhancing binding and activity of the USP16 deubiquitinase at transcribed genes. [UniProt]

Description: Serine/threonine-protein kinase component of the chromosomal passenger complex (CPC), a complex that acts as a key regulator of mitosis. The CPC complex has essential functions at the centromere in ensuring correct chromosome alignment and segregation and is required for chromatin-induced microtubule stabilization and spindle assembly. Involved in the bipolar attachment of spindle microtubules to kinetochores and is a key regulator for the onset of cytokinesis during mitosis. Required for central/midzone spindle assembly and cleavage furrow formation. Key component of the cytokinesis checkpoint, a process required to delay abscission to prevent both premature resolution of intercellular chromosome bridges and accumulation of DNA damage: phosphorylates CHMP4C, leading to retain abscission-competent VPS4 (VPS4A and/or VPS4B) at the midbody ring until abscission checkpoint signaling is terminated at late cytokinesis. AURKB phosphorylates the CPC complex subunits BIRC5/survivin, CDCA8/borealin and INCENP. Phosphorylation of INCENP leads to increased AURKB activity. Other known AURKB substrates involved in centromeric functions and mitosis are CENPA, DES/desmin, GPAF, KIF2C, NSUN2, RACGAP1, SEPT1, VIM/vimentin, GSG2/Haspin, and histone H3. A positive feedback loop involving GSG2 and AURKB contributes to localization of CPC to centromeres. Phosphorylation of VIM controls vimentin filament segregation in cytokinetic process, whereas histone H3 is phosphorylated at 'Ser-10' and 'Ser-28' during mitosis (H3S10ph and H3S28ph, respectively). A positive feedback between GSG2 and AURKB contributes to CPC localization. AURKB is also required for kinetochore localization of BUB1 and SGOL1. Phosphorylation of p53/TP53 negatively regulates its transcriptional activity. Key regulator of active promoters in resting B- and T-lymphocytes: acts by mediating phosphorylation of H3S28ph at active promoters in resting B-cells, inhibiting RNF2/RING1B-mediated ubiquitination of histone H2A and enhancing binding and activity of the USP16 deubiquitinase at transcribed genes. [UniProt]

Description: Chromosomal segregation during mitosis as well as meiosis is regulated by kinases and phosphatases. The Aurora kinases associate with microtubules during chromosome movement and segregation. STK12 (Aurora kinase B) localizes to microtubules near kinetochores, specifically to the specialized microtubules called K-fibers, and Aurora kinase A localizes to centrosomes

Description: Chromosomal segregation during mitosis as well as meiosis is regulated by kinases and phosphatases. The Aurora kinases associate with microtubules during chromosome movement and segregation. STK12 (Aurora kinase B) localizes to microtubules near kinetochores, specifically to the specialized microtubules called K-fibers, and Aurora kinase A localizes to centrosomes

Description: Available in various conjugation types.

Description: Available in various conjugation types.

Description: Available in various conjugation types.

Description: Additional name(s) for this target protein: AURKB; aurora kinase B antibody; AIK2

Description: Aurora kinase A, also called ARK1, AURKA, AIK , AURORA2 ,BTAK, PPP1R47, STK7, STK15, and STK6, is a mitotic centrosomal protein kinase. The main role of AURKA in tumor development is in controlling chromosome segregation during mitosis. Aurora A is a member of a family of mitotic serine/threonine kinases. Cell cycle and Northern blot analyses showed that peak expression of the protein occurs during the G2/M phase and then decreases. By fluorescence in situ hybridization, the gene is represented by 2 signals in chromosome bands 20q13.2-q13.3 and 1q41-q42. It is overexpressed in many human cancers. Ectopic overexpression of Aurora A in mammalian cells induces centrosome amplification, chromosome instability, and oncogenic transformation, a phenotype characteristic of loss-of-function mutations of p53. Depletion of Ajuba prevented activation of AURKA at centrosomes in late G2 phase and inhibited mitotic entry. Activation of the kinase was independently sufficient to induce rapid ciliary resorption, and AURKA acted in this process through phosphorylation of HDAC6, leading to HDAC6-dependent tubulin deacetylation and destabilization of the ciliary axoneme.

Description: Aurora kinase B, also called Aik2, AIM-1, ARK2, AurB, STK12, IPL1, PPP1R48 or STK5, localizes to microtubules near kinetochores, specifically to the specialized microtubules called K-fibers. Cell cycle and Northern blot analyses showed that AURKB is expressed in the S phase and persistently thereafter. Western blot analysis indicated that it is localized in the midbodies during anaphase. Northern blot analysis detected strong expression of a 1.5-kb transcript in thymus, with weaker expression in small intestine, testis, colon, spleen, and brain. Examination of the role of both kinases in the phosphorylation of CENPA revealed that the reaction is mediated sequentially by AURKA and AURKB in early mitosis. EB1 overexpression enhanced AURKB kinase activity, and knockdown of EB1 with small interfering RNA impaired AURKB activity. EB1 protected Aurora B from dephosphorylation/inactivation by protein phosphatase-2A by blocking binding of PP2A.

Description: Available in various conjugation types.