Proteins & Peptides

HSP70 is a member of the heat shock protein family and is synthesized by cells of many organisms in response to stress (1). HSP70 is found mostly but not exclusively in the nucleus of unstressed cells. For several hours after a short heat shock, however, it is strongly concentrated in nucleoli (2). Nucleoli are transiently damaged by such a heat shock: their morphology changes and assembly and export of ribosomes is blocked for several hours. HSP70 helps to stabilize the morphological changes of the nucleoli. HSP70 Protein is ideal for investigators involved in Signaling Proteins, Cell Stress & Chaperone Proteins, Apoptosis/Autophagy, Cancer, and Cellular Stress research.

HSP70 is a member of the heat shock protein family and is synthesized by cells of many organisms in response to stress (1). HSP70 is found mostly but not exclusively in the nucleus of unstressed cells. For several hours after a short heat shock, however, it is strongly concentrated in nucleoli (2). Nucleoli are transiently damaged by such a heat shock: their morphology changes and assembly and export of ribosomes is blocked for several hours. HSP70 helps to stabilize the morphological changes of the nucleoli. HSP70 Protein is ideal for investigators involved in Signaling Proteins, Cell Stress & Chaperone Proteins, Apoptosis/Autophagy, Cancer, and Cellular Stress research.

IkB-alpha is an inhibitor of the NFkB complex and inactivates the NFkB by trapping it in the cytoplasm (1). Phosphorylation of serine residues on the IkB protein by IkB kinases (IKKs) marks it for destruction via the ubiquitination pathway, thereby allowing the activation of the NFkB complex. Synthetic glucocorticoid such as dexamethasone display anti-inflammatory effects by inducing the increased synthesis of the IkB protein thereby inhibiting the activity of the NFkB complex. Overexpression of the IkB-alpha gene in fibroblasts leads to inhibition of production of IL-6, TNF receptor, MMP-1, MMP-3 and MMP-13 (2). IkB-alpha Protein is ideal for investigators involved in Signaling Proteins, Transcription Proteins, AKT/PKB Pathway, Apoptosis/Autophagy, Inflammation, and p38 Pathway research.

IkB-alpha is an inhibitor of the NFkB complex and inactivates the NFkB by trapping it in the cytoplasm (1). Phosphorylation of serine residues on the IkB protein by IkB kinases (IKKs) marks it for destruction via the ubiquitination pathway, thereby allowing the activation of the NFkB complex. Synthetic glucocorticoid such as dexamethasone display anti-inflammatory effects by inducing the increased synthesis of the IkB protein thereby inhibiting the activity of the NFkB complex. Overexpression of the IkB-alpha gene in fibroblasts leads to inhibition of production of IL-6, TNF receptor, MMP-1, MMP-3 and MMP-13 (2). IkB-alpha Protein is ideal for investigators involved in Signaling Proteins, Transcription Proteins, AKT/PKB Pathway, Apoptosis/Autophagy, Inflammation, and p38 Pathway research.

IkB-alpha is an inhibitor of the NFkB complex and inactivates the NFkB by trapping it in the cytoplasm (1). Phosphorylation of serine residues on the IkB protein by IkB kinases (IKKs) marks it for destruction via the ubiquitination pathway, thereby allowing the activation of the NFkB complex. Synthetic glucocorticoid such as dexamethasone display anti-inflammatory effects by inducing the increased synthesis of the IkB protein thereby inhibiting the activity of the NFkB complex. Overexpression of the IkB-alpha gene in fibroblasts leads to inhibition of production of IL-6, TNF receptor, MMP-1, MMP-3 and MMP-13 (2). IkB-alpha Protein is ideal for investigators involved in, Signaling Proteins, Transcription Proteins, AKT/PKB Pathway, Apoptosis/Autophagy, Inflammation, and p38 Pathway research.

IkB-alpha is an inhibitor of the NFkB complex and inactivates the NFkB by trapping it in the cytoplasm (1). Phosphorylation of serine residues on the IkB protein by IkB kinases (IKKs) marks it for destruction via the ubiquitination pathway, thereby allowing the activation of the NFkB complex. Synthetic glucocorticoid such as dexamethasone display anti-inflammatory effects by inducing the increased synthesis of the IkB protein thereby inhibiting the activity of the NFkB complex. Overexpression of the IkB-alpha gene in fibroblasts leads to inhibition of production of IL-6, TNF receptor, MMP-1, MMP-3 and MMP-13 (2). IkB-alpha Protein is ideal for investigators involved in, Signaling Proteins, Transcription Proteins, AKT/PKB Pathway, Apoptosis/Autophagy, Inflammation, and p38 Pathway research.

IkB-beta is part of the NFkB complex and it inactivates NFkB complex by binding to it and trapping it in the cytoplasm. Phosphorylation of serine residues on IkB-beta mediated by IkB kinases leads to its destruction via the ubiquitination pathway thereby allowing activation of the NFkB complex which translocates into the nucleus and binds DNA at kappa-B-binding motifs (1). The PEST domain of IkB-beta can interact with two proteins KBRAS1 and KBRAS2 and this interaction can decrease the rate of degradation IkB-beta. IkBβ has been shown to participate in multiple signaling pathways including adipocytokine signaling pathway, B-cell receptor signaling pathway, T-cell receptor signaling pathway and Hypoxia (2). IkB-beta Protein is ideal for investigators involved in Signaling Proteins, Transcription Proteins, AKT/PKB Pathway, Apoptosis/Autophagy, Inflammation, and p38 Pathway research.

IkB-beta is part of the NFkB complex and it inactivates NFkB complex by binding to it and trapping it in the cytoplasm. Phosphorylation of serine residues on IkBβ mediated by IkB kinases leads to its destruction via the ubiquitination pathway thereby allowing activation of the NFkB complex which translocates into the nucleus and binds DNA at kappa-B-binding motifs (1). The PEST domain of IkBβ can interact with two proteins KBRAS1 and KBRAS2 and this interaction can decrease the rate of degradation IkBβ. IkBβ has been shown to participate in multiple signaling pathways including adipocytokine signaling pathway, B-cell receptor signaling pathway, T-cell receptor signaling pathway and Hypoxia (2). IkBβ Protein is ideal for investigators involved in Signaling Proteins, Transcription Proteins, AKT/PKB Pathway, Apoptosis/Autophagy, Inflammation, and p38 Pathway research.

INCENP or inner centromere protein antigens 135/155kDa is a constitutively binding centromere proteins and 'passenger,' or transiently interacting, proteins. The overexpression of a truncation mutant of chicken INCENP and a chimeric CENPB:INCENP protein in mammalian cell culture disrupted both prometaphase chromosome alignment and completion of cytokinesis (1). INCENP forms a complex with the evolutionarily conserved family of Aurora B kinases which helps coordinate chromosome segregation, spindle behavior, and cytokinesis during mitosis (2). INCEP Protein is ideal for investigators involved in Signaling Proteins, Microtubule/Actin Associated Proteins, Cell Cycle, and Invasion/Metastasis research.