Recombinant Human Alkaline phosphatase, placental type(ALPP),partial Reference: CSB-BP001632HU1_100 In most mammals there are four different isozymes: placental, placental-like, intestinal and tissue non-specific (liver/bone/kidney).
Recombinant Human Alkaline phosphatase, placental type(ALPP),partial Reference: CSB-BP001632HU1_10 In most mammals there are four different isozymes: placental, placental-like, intestinal and tissue non-specific (liver/bone/kidney).
Recombinant Macaca fascicularis Apolipoprotein C-III(APOC3) Reference: CSB-BP001933MOV_1 Component of triglyceride-rich very low density lipoproteins (VLDL) and high density lipoproteins (HDL) in plasma. Plays a multifaceted role in triglyceride homeostasis. Intracellularly, promotes hepatic very low density lipoprotein 1 (VLDL1) assembly and secretion; extracellularly, attenuates hydrolysis and clearance of triglyceride-rich lipoproteins (TRLs). Impairs the lipolysis of TRLs by inhibiting lipoprotein lipase and the hepatic uptake of TRLs by remnant receptors. Formed of several curved helices connected via semiflexible hinges, so that it can wrap tightly around the curved micelle surface and easily adapt to the different diameters of its natural binding partners.
Recombinant Macaca fascicularis Apolipoprotein C-III(APOC3) Reference: CSB-BP001933MOV_100 Component of triglyceride-rich very low density lipoproteins (VLDL) and high density lipoproteins (HDL) in plasma. Plays a multifaceted role in triglyceride homeostasis. Intracellularly, promotes hepatic very low density lipoprotein 1 (VLDL1) assembly and secretion; extracellularly, attenuates hydrolysis and clearance of triglyceride-rich lipoproteins (TRLs). Impairs the lipolysis of TRLs by inhibiting lipoprotein lipase and the hepatic uptake of TRLs by remnant receptors. Formed of several curved helices connected via semiflexible hinges, so that it can wrap tightly around the curved micelle surface and easily adapt to the different diameters of its natural binding partners.
Recombinant Macaca fascicularis Apolipoprotein C-III(APOC3) Reference: CSB-BP001933MOV_20 Component of triglyceride-rich very low density lipoproteins (VLDL) and high density lipoproteins (HDL) in plasma. Plays a multifaceted role in triglyceride homeostasis. Intracellularly, promotes hepatic very low density lipoprotein 1 (VLDL1) assembly and secretion; extracellularly, attenuates hydrolysis and clearance of triglyceride-rich lipoproteins (TRLs). Impairs the lipolysis of TRLs by inhibiting lipoprotein lipase and the hepatic uptake of TRLs by remnant receptors. Formed of several curved helices connected via semiflexible hinges, so that it can wrap tightly around the curved micelle surface and easily adapt to the different diameters of its natural binding partners.
Recombinant Mouse Apolipoprotein E(Apoe) Reference: CSB-BP001936MO_1 APOE knockout mice display severe hypercholesterolemia associated with impaired clearance of dietary fats. Excess cholesterol is more particularly associated with the atherogenic very low and intermediate density lipoproteins in the plasma. These mice are therefore prone to atherosclerosis. Animals with a double knockout of APOE and CD36, fed a Western diet for 12 weeks, exhibit much lower levels of CXCL1, CXCL2 and CCL5 mRNA expression in the descending aorta and a corresponding decrease in atherosclerotic lesion formation, compared to APOE single knockout mice. Animals with a double knockout of APOE and TLR4 or TLR6 also have less aortic plaque formation than single knockout mice. All 3 double knockout show lower serum concentrations of IL1A, ILB and IL18.
Recombinant Mouse Apolipoprotein E(Apoe) Reference: CSB-BP001936MO_100 APOE knockout mice display severe hypercholesterolemia associated with impaired clearance of dietary fats. Excess cholesterol is more particularly associated with the atherogenic very low and intermediate density lipoproteins in the plasma. These mice are therefore prone to atherosclerosis. Animals with a double knockout of APOE and CD36, fed a Western diet for 12 weeks, exhibit much lower levels of CXCL1, CXCL2 and CCL5 mRNA expression in the descending aorta and a corresponding decrease in atherosclerotic lesion formation, compared to APOE single knockout mice. Animals with a double knockout of APOE and TLR4 or TLR6 also have less aortic plaque formation than single knockout mice. All 3 double knockout show lower serum concentrations of IL1A, ILB and IL18.
Recombinant Mouse Apolipoprotein E(Apoe) Reference: CSB-BP001936MO_20 APOE knockout mice display severe hypercholesterolemia associated with impaired clearance of dietary fats. Excess cholesterol is more particularly associated with the atherogenic very low and intermediate density lipoproteins in the plasma. These mice are therefore prone to atherosclerosis. Animals with a double knockout of APOE and CD36, fed a Western diet for 12 weeks, exhibit much lower levels of CXCL1, CXCL2 and CCL5 mRNA expression in the descending aorta and a corresponding decrease in atherosclerotic lesion formation, compared to APOE single knockout mice. Animals with a double knockout of APOE and TLR4 or TLR6 also have less aortic plaque formation than single knockout mice. All 3 double knockout show lower serum concentrations of IL1A, ILB and IL18.
Recombinant Streptococcus pyogenes serotype M1 Adenine... Reference: CSB-BP001954SMT_100 Catalyzes a salvage reaction resulting in the formation of AMP, that is energically less costly than de novo synthesis.
Recombinant Streptococcus pyogenes serotype M1 Adenine... Reference: CSB-BP001954SMT_20 Catalyzes a salvage reaction resulting in the formation of AMP, that is energically less costly than de novo synthesis.
Recombinant Human AT-rich interactive domain-containing protein... Reference: CSB-BP002058HU1_100 Involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Binds DNA non-specifically. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a post-mitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to post-mitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth
Recombinant Human AT-rich interactive domain-containing protein... Reference: CSB-BP002058HU1_10 Involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Binds DNA non-specifically. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a post-mitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to post-mitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth