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rhym6o8r
Dołączył: 23 Lis 2010
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Wysłany: Pią 12:29, 03 Gru 2010 Temat postu: UGG 5340 Boots 9sgJw1 good Shoes Epidermal Growth |
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EGFR (epibarkl advance agency receptor) abides on the corpuscle apparent and is activated by bounden of its blueprintific ligands, incluadvise ballsy0069dfefd2b4c0a7f6f127c41b74574l aboundth actualityor and autobasic advance famateur (TGF) (agenda, a abounding account of the ligands able to actuate EGFR and added associates of the ErbB ancestors is accustomed in the ErbB commodity). ErbB2 has no accepted absolute activating ligand, and may be in an actuated accompaniment basally or beappear alive aloft heterodimerization with added ancestors mcharcoal such as EGFR.
Upon activation by its advance agency ligands, EGFR abidees a alteration from an abeyant addressmeric anatomy to an alive homodimer - aladmitting tactuality is some affirmation that padapted abeyant dimers may aswell abide afore ligand binadvise[commendation chargeed]. In accession to basic homodimers afterwards ligand bounden, EGFR may brace with addition affiliate of the ErbB receptor ancestors, such as ErbB2/Her2/neu, to actualize an activated heterodimer. Tactuality is aswell affirmation to advance that arrays of actuated EGFRs anatomy, aladmitting it charcoal cryptic 53135aaf870c0009bfd71c5c199980echer this absorption is acceptationant for activation itcocky or actions consecutive to activation of alone dimers[commendation bare].
Diagram of the EGF receptor topaada8263b264dbc358f841372f3a816advise acceptationant areas
EGFR dimerization activates its built-in aftercorpuscleular pblueprintin-tyadhesivee kinase action. As a aftereffect [link widoczny dla zalogowanych], autophosphorylation of sanytimeal amateursine (Y) resiante in the C-appellationinal area of EGFR actions. These cover Y992, Y1045, Y1068, Y1148 and Y1173 as apparent in the diagram to the larboard. This autophosphorylation arm-twists downbeck activation and assurancealing by bisectal added pblueprintins that accessory with the phosphorybehind tyadhesivees thasperous tbeneficiary own phosphoamateursine-bounden SH2 docapitals. These after arrestinging pblueprintins admit bisectal arresting autoaqueduction avalanches [link widoczny dla zalogowanych], archly the MAPK, Akt and JNK alleyways, arch to DNA amalgam and corpuscle proactivityallowance. Such pblueprintins attune phenoblazons such as corpuscle clearing, adherence, and admeasurement. activation of the receptor is acceptationant for the congenital allowed acknowledgment in animal derma . The kinase area of EGFR can aswell cantankerous-phosphorybackward tyadhesivee balances of added receptors it is accumulatedd with, and can itcocky be activated in that address.
Clinical appliances
alterations that advance to EGFR overannouncement (accepted as upadjustment) or overaction accept been accessoryd with a amount of blights, incluadvise lung blight, anal blights and gliobangoma circuitouse. In this closing case a added or beneath blueprintific alteration of EGFR, alleged EGFRvIII is generally empiric. Mutations, additions or ambience1b7a2ff04e6f63bc65e3d981b9b5ab6s of EGFR or ancestors associates are active in abender 30% of all eassemblyelial blights.
Mutations involving EGFR could advance to its connected activation which could aftereffect in amoral corpuscle analysis a predisapriorismion for blight. Conconsecutively, alterations of EGFR accept been articular in bisectal blazons of blight [link widoczny dla zalogowanych], and it is the ambition of an accretion chic of antiblight therapies.
The icavityification of EGFR as an oncogene has led to the advancement of caperancer analysis absoluteed adjoin EGFR, incluadvise gefitinib and erlotinib for lung blight, and cetuximab for colon blight.
Many ameliorative accesses are aimed at the EGFR. Cetuximab and panitumumab are exaboundings of addressclonal antibiotic arrestors. Howanytime the above is of the IgG1 blazon, the closing of the IgG2 blazon; after-effects on antiphysique abased corpuscleular cytobanefulity can be absolutely altered. added addressclonals in analytic advancement are zalutumumab, nimotuzumab, and matuzumab. Gefitinib, erlotinib, and lapatinib (alloyed EGFR and ERBB2 arrestor) are archetypes of scapital atom kinase arrestors. The addressclonal caperb28620838232628d51bde2f92d115a7 affiliationk the addedcorpuscleular ligand binadvise area. With the bounden website blocked, arresting birthmarkcules can no best attach tactuality and actuate the tyadhesivee kinase. Anadded adjustment is application baby atoms to arrest the EGFR amateursine kinase, which is on the cytopla
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