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Binding activity

Motor proteins move along MTs in an ATP-dependent manner. Members of the superfamily of kinesin motors move only to the plus ends and dynein motors only to the minus ends. The respective motor domains are linked via adaptor proteins to their cargoes. The binding activity of the motors to MTs is regulated by kinases and phosphatases. When motors are immobilized at their cargo-binding area, they can move MTs. [Pg.415]

Besides the cytokine receptors that lack intrinsic kinase activity but have associated JAK kinases, STAT proteins can be activated by a variety of G-protein coupled receptors and growth factor receptors with intrinsic tyrosine kinase activity (for example EGF, PDGF, CSF-1, and angiotensin receptor). Increasing evidence suggests a critical role for STAT family members in oncogenesis and aberrant cell proliferation. Constitutively activated STATs have been found in many transformed cell lines and a wide variety of human tumor entities. Numerous non-receptor tyrosine kinases and viral oncoproteins, such as v-Src, v-Abl, v-Sis, and v-Eyk, have been identified to induce DNA-binding activity of STAT proteins. [Pg.669]

NFAT was initially identified in activated T cells as a DNA binding activity required for IL-2 expression, a cytokine that plays a key role in T cell activation and survival. Subsequent studies revealed the involvement... [Pg.848]

Beside other functions in signal transduction, protein inhibitors of activated STAT suppress the DNA-binding activity of STAT proteins. [Pg.977]

The human HS cycle can be considered broadly as a period which leads to the dramatic shift in activities of the transcriptional and translational machinery followed by eventual recovery and resumption of original activities preceding stress. Figure 1 depicts many of the key events in the HS cycle for a typical human cell line such as cervical carcinoma-derived HeLa cells. Most cells respond in an identical fashion, but some cell types that have distinctive HS responses. These differences are manifested by shifts in the relative concentrations of accumulated HS proteins and possibly in the pattern of posttranslational modifications. In all cases, however, the cellular stress response is heralded by induction of a specific transcription factor whose DNA binding activity facilitates increased expression of one or more of the stress-inducible genes. [Pg.413]

HSFl phosphorylation must be sensitive to nonheat inducers of HSF-DNA binding activity because HSFl phosphorylation can be achieved at 37 °C by other inducers of the HS response. HSF 1 contains polypeptide sequences that could serve as substrates for well characterized protein kinases, but few of these are known to be heat inducible. One family of protein kinases, the S6 protein kinases, have already been shown to exhibit heat inducible activity however, their peak level of activity during HS occurs well after the maximal induction of HSF phosphorylation (Jurivich et al., 1991). Thus, other protein kinases are likely to be directly linked to the phosphorylation of HSF. Some of the putative protein phosphorylation sites on HSF include motifs for protein kinase C, casein kinase, and enterokinase. There are tyrosine sequences that match substrates for known tyrosine kinases, but whether these residues are accessible to phosphorylation is not established. [Pg.421]

Mosser, D.D., Theodorakis, N.G., Morimoto, R.I. (1988). Coordinate changes in heat shock element binding activity and hsp70 gene transcription rates in human cells. Mol. Cell. Biol. 8,4736-4744. [Pg.458]

Mosser, D.D., Duchaine, J., Massie, B. (1993). The DNA binding activity of the human heat shock transcription factor is regulated in vivo by hsp70. Mol. Cell. Biol. 13, 5427-5438. [Pg.458]

Sarge, K.D., Murphy, S.P., Morimoto, R.l. (1993). Activation of heat shock gene transcription by heat shock factor 1 involves oligomenzation, acquisition of DNA binding activity, and nuclear localization and can occur in the absence of stress. Mol. Cell. Biol. 13. 1392-1407. [Pg.459]

Helicase has also been a focal point for the development of antiviral chemotherapy of the coronavirus associated with severe acute respiratory syndrome (SARS) in humans. Although several experimental compounds with nucleic acid binding activity showing effective inhibition of SARS-CoV helicase were reported in 2005, there have been no reports of any further development since that time (Kesel 2005). It remains to be seen whether the S ARS-CoV compounds will be developed further, especially since no new infections have been observed in recent years. [Pg.164]

K.M., Griesser, H.J., Kwak, J., Goodman, M., and Steele, J.G. Peptoid-con-taining collagen mimetics with cell binding activity. J. Biomed. Mater. Res. 2000,... [Pg.31]

Active with a measured binding activity or inactive... [Pg.335]

Let A = yc, , 1 < / < Nc, be conformations generated for C using a computational method. Because the global free energy minimum conformation is expected to statistically dominate the thermodynamic ensemble, the predicted binding activity for C is determined by (C)=min F y. ) = F(yf ). [Pg.336]

Comparison of the binding activities of the proteins that contain these motifs leads to several important generalizations. [Pg.388]


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See also in sourсe #XX -- [ Pg.56 , Pg.59 ]

See also in sourсe #XX -- [ Pg.217 ]




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Activation energy binding energies

Activation of DNA binding

Active Sites and Substrate Binding Models

Active binding analysis

Active-site binding

Activity and protein binding

Activity binding affinity contrasted

Activity enzyme-binding experiment

Activity ligand-binding

Activity, guest binding

Agonists binding and activation

Anti-inflammatory Activities of Omalizumab (Xolair), a Recombinant Humanized Monoclonal Antibody Binding IgE

Binding activation energy

Binding of Catalytically Active Complexes

Binding protein ATPase activity

Co-activator binding

Covalent Binding to Activated Nonactivated Surfaces

Covalent binding activation

DNA binding activities

DNA binding activities polymerase

Dioxygen Binding and Activation Reactive Intermediates

Estrogen receptor binding activity

Folates binding activity

Folic acid binding activity

GABAa receptors, activation barbiturate binding site

GABAa receptors, activation benzodiazepine binding site

GABAa receptors, activation binding affinities

Inhibitors Bind at the Active Site

Iron Regulatory Protein-1 RNA-Binding Activity

Ligand Binding and Activation

Ligand Binding and Activation of CAR

Ligand Binding, Activation and Corepression of the RXR-Heterodimers

Ligand binding activation step

Molecular Oxygen Binding and Activation Oxidation Catalysis

Mouse vas deferens activity in receptor binding assa

Peroxisome proliferator activated receptor binding protein

Platelet-activating factor , binding

Platelet-activating factor , binding sites

Platelet-activating factor , binding structure

Platelet-activating factor , binding synthesis

Potassium channel activators binding studies

Potassium channel activators ligand binding

Protease Inhibitors that Bind to One Side of the Active Site

Quantitative structure-activity relationship estrogen receptor binding affinity

Receptor binding assay activity

Secondary active transporters binding protein dependent

Specific Amino Acids at the Active-Site Involved in Catalysis and Substrate Binding

Sterically active binding sites

Sterol regulatory element-binding protein SREBP-1 pathway activation

Structural Determinants of Ligand Binding and Receptor Activation by CC Chemokines

Substrate binding active ternary complex

Substrate binding at an active site

Sulfate binding protein active site

Sulfhydryl groups, metal binding active site

Tannin activity protein binding

The Binding and Activation Steps

The Distinction between Agonist Binding and Receptor Activation

The Law of Mass Action, binding sites and receptors—understanding why specific, potent biological activity is a rare property for any one chemical to possess

Transposons binding activity

Upstream binding factor activation

Virus Sialidase Substrate Binding and Active Site

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