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NF-κB and has
Due to its role in generating the activated form of NF-κB, an anti-apoptotic and pro-inflammatory regulator of cytokine expression, proteasomal activity has been linked to inflammatory and autoimmune diseases.
It has been shown to reduce inflammation: troglitazone use was associated with a decrease of nuclear factor kappa-B ( NF-κB ) and a concomitant increase in its inhibitor ( IκB ).
One of the proteins – WSSV449 – has some similarity to host protein Tube and can function like Tube by activating the NF-κB pathway.
Incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development.
NF-κB has also been implicated in processes of synaptic plasticity and memory .< ref name =" Albensi_2000 ">

NF-κB and found
have found that the root of the plant is able to reduce the activity of NF-κB in rats.
NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens.

NF-κB and role
NF-κB plays a key role in regulating the immune response to infection ( kappa light chains are critical components of immunoglobulins ).

NF-κB and on
* They act on DNA ( activating or inhibiting transcription factors such as NF-κB, which is linked to pro-inflammatory cytokine production )

NF-κB and cell
Akt also activates IKKα, which leads to NF-κB activation and cell survival.
NF-κB is a heterodimeric transcription factor that translocates to the nucleus and mediates the transcription of a vast array of proteins involved in cell survival and proliferation, inflammatory response, and anti-apoptotic factors.
By binding RANKL, OPG inhibits nuclear kappa B ( NF-κB ) which is a central and rapid acting transcription factor for immune-related genes, and a key regulator of inflammation, innate immunity, and cell survival and differentiation.
Keratinocytes engineered to not express alpha-catenin have disrupted cell adhesion and activated NF-κB.
NF-κB regulates nuclear gene transcription to promote cell survival.
The DNA / NF-κB complex then recruits other proteins such as coactivator ( genetics ) | coactivators and RNA polymerase, which transcribe downstream DNA into mRNA, which, in turn, is translated into protein, which results in a change of cell function.

NF-κB and type
* 1996: A molecular pathway ( called NF-κB ) is identified in fat and the liver that is activated by obesity ( and a fatty diet ) and causes the insulin resistance that can lead to type 2 diabetes ( Steven E. Shoelson, M. D., Ph. D .).
It recognizes dsRNA associated with viral infection, and induces the activation of NF-κB and the production of type I interferons.
Upon recognition, TLR 3 induces the activation of NF-κB to increase production of type I interferons which signal other cells to increase their antiviral defenses.

NF-κB and .
Active NF-κB induces the expression of anti-apoptotic genes such as Bcl-2, resulting in inhibition of apoptosis.
After binding dsRNA, this receptor activates the transcription factors IRF3 and NF-κB, which are important for initiating synthesis of many inflammatory proteins.
Certain transcription factors regulating the expression of specific genes, including one component of the mammalian complex NF-κB, are synthesized as inactive precursors whose ubiquitination and subsequent proteasomal degradation converts them to an active form.
The proteasomal activation of NF-κB by processing p105 into p50 via internal proteolysis is one major example.
Some of these molecules like NOD2 interact with RIP2 kinase that activates NF-κB signaling, whereas others like NALP3 interact with inflammatory caspases and initiate processing of particular cytokines like interleukin-1β.
Nine-amino-acid transactivation domain ( 9aaTAD ) defines a novel domain common to a large superfamily of eukaryotic transcription factors represented by Gal4, Oaf1, Leu3, Rtg3, Pho4, Gln3, Gcn4 in yeast and by p53, NFAT, NF-κB and VP16 in mammals.
9aaTAD transcription factors p53, VP16, MLL, E2A, HSF1, NF-IL6, NFAT1 and NF-κB interact directly with the general coactivators TAF9 and CBP / p300.
Other important breakthroughs from Baltimore's lab include the discovery of the transcription factor NF-κB and the recombination activating genes RAG-1 and RAG-2.
Recently, it was shown that bile acids are able to induce intestinal differentiation, in gastroesophageal junction cells, through inhibition of the Epidermal growth factor receptor ( EGFR ) receptor which results in inhibition of Akt, upregulation of the p50 subunit of NF-κB ( NFKB1 ) and ultimately activation of the promotor of the homeobox gene CDX2.
Phagocytosis in mammalian immune cells is activated by attachment to Pathogen-associated molecular patterns ( PAMPS ), which leads to NF-κB activation.
Hypoxia also causes reactive oxygen species ( ROS ) production that can activate HIF-1, EGR-1, and nuclear factor-κB ( NF-κB ), which regulates HIF-1 transcription.
* Activation of NF-κB: TRADD recruits TRAF2 and RIP.
An inhibitory protein, IκBα, that normally binds to NF-κB and inhibits its translocation, is phosphorylated by IKK and subsequently degraded, releasing NF-κB.
Its death-inducing capability is weak compared to other family members ( such as Fas ), and often masked by the anti-apoptotic effects of NF-κB.
For instance, NF-κB enhances the transcription of C-FLIP, Bcl-2, and cIAP1 / cIAP2, inhibitory proteins that interfere with death signaling.
On the other hand, activated caspases cleave several components of the NF-κB pathway, including RIP, IKK, and the subunits of NF-κB itself.
The mechanism involves the formation of reactive oxygen species leading to upregulation of the transcription factor NF-κB.
NF-κB is a known regulator of the genes that encode cytokines, and cytokine receptors.

has and been
Besides I heard her old uncle that stays there has been doin' it ''.
Southern resentment has been over the method of its ending, the invasion, and Reconstruction ; ;
The situation of the South since 1865 has been unique in the western world.
The North should thank its stars that such has been the case ; ;
As it is, they consider that the North is now reaping the fruits of excess egalitarianism, that in spite of its high standard of living the `` American way '' has been proved inferior to the English and Scandinavian ways, although they disapprove of the socialistic features of the latter.
In what has aptly been called a `` constitutional revolution '', the basic nature of government was transformed from one essentially negative in nature ( the `` night-watchman state '' ) to one with affirmative duties to perform.
For lawyers, reflecting perhaps their parochial preferences, there has been a special fascination since then in the role played by the Supreme Court in that transformation -- the manner in which its decisions altered in `` the switch in time that saved nine '', President Roosevelt's ill-starred but in effect victorious `` Court-packing plan '', the imprimatur of judicial approval that was finally placed upon social legislation.
Labor relations have been transformed, income security has become a standardized feature of political platforms, and all the many facets of the American version of the welfare state have become part of the conventional wisdom.
Historically, however, the concept is one that has been of marked benefit to the people of the Western civilizational group.
In recent weeks, as a result of a sweeping defense policy reappraisal by the Kennedy Administration, basic United States strategy has been modified -- and large new sums allocated -- to meet the accidental-war danger and to reduce it as quickly as possible.
The malignancy of such a landscape has been beautifully described by the Australian Charles Bean.
There has probably always been a bridge of some sort at the southeastern corner of the city.
Even though in most cases the completion of the definitive editions of their writings is still years off, enough documentation has already been assembled to warrant drawing a new composite profile of the leadership which performed the heroic dual feats of winning American independence and founding a new nation.
Madison once remarked: `` My life has been so much a public one '', a comment which fits the careers of the other six.
Thus we are compelled to face the urbanization of the South -- an urbanization which, despite its dramatic and overwhelming effects upon the Southern culture, has been utterly ignored by the bulk of Southern writers.
But the South is, and has been for the past century, engaged in a wide-sweeping urbanization which, oddly enough, is not reflected in its literature.
An example of the changes which have crept over the Southern region may be seen in the Southern Negro's quest for a position in the white-dominated society, a problem that has been reflected in regional fiction especially since 1865.
In the meantime, while the South has been undergoing this phenomenal modernization that is so disappointing to the curious Yankee, Southern writers have certainly done little to reflect and promote their region's progress.
Faulkner culminates the Southern legend perhaps more masterfully than it has ever been, or could ever be, done.
The `` approximate '' is important, because even after the order of the work has been established by the chance method, the result is not inviolable.
But it has been during the last two centuries, during the scientific revolution, that our independence from the physical environment has made the most rapid strides.
In the life sciences, there has been an enormous increase in our understanding of disease, in the mechanisms of heredity, and in bio- and physiological chemistry.
Even in domains where detailed and predictive understanding is still lacking, but where some explanations are possible, as with lightning and weather and earthquakes, the appropriate kind of human action has been more adequately indicated.
The persistent horror of having a malformed child has, I believe, been reduced, not because we have gained any control over this misfortune, but precisely because we have learned that we have so little control over it.

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