Protein function Dotaz Zobrazit nápovědu
1st ed. xvi, 310 s. : il.
- Konspekt
- Biochemie. Molekulární biologie. Biofyzika
- NLK Obory
- biochemie
F -- Contents -- Preface xi -- 1 Introduction to Protein Engineering 1 -- Jeffrey L. Craik -- 2 Protein Conformation 33 -- Fred E. Cohen and David P. on Protein Folding: Methodology, Application, -- and Interpretation 249 -- Mark R. Robert Matthews -- 10 Successful Protein Folding on an Industrial Scale 283 -- Rainer Rudolph -- • • Structure-Function Relationships for Protein Design 317 -- Craig S.
x, 518 s. : il.
- Klíčová slova
- Biologie molekulární, Proteiny,
- MeSH
- molekulární biologie MeSH
- proteiny MeSH
Protein Requirements of Adults . 140 -- IV. Renal Function, Food, and Growth . 238 -- References 241 -- CHAPTER 17 -- PROTEIN METABOLISM AND REQUIREMENTS Loss ňf Cell Function vs. Cell Death . 255 -- X. Protein Intake and Disease . 302 -- VII. Protein Malnutrition in Adults . 560 -- References 561 -- CHAPTER 23 -- PROTEIN DEFICIENCY AND INFECTIVE
15, 642 s. : il., tab.
- Klíčová slova
- Metabolismus, Proteiny,
- MeSH
- metabolismus MeSH
- proteiny MeSH
- Konspekt
- Biochemie. Molekulární biologie. Biofyzika
- NLK Obory
- biochemie
- vnitřní lékařství
C-reaktivní protein je markerem aktivity zánětlivé odpovědi, která se podílí na rozvoji aterosklerózy a jejích klinických komplikací. Současně je C-reaktivní protein i aktivním účastníkem neboli mediátorem této zánětlivé reakce. Na samém počátku aterosklerotického procesu má ale C-reaktivní protein ochranné, antiaterosklerotické působení. Oba aspekty působení CRP, tedy prozánětlivý i protizánětlivý, spočívají v rozsahu jeho spolupráce s komplementovým systémem. Z vývojového hlediska je prvotním účinkem protizánětlivé působení CRP, které usnadňuje odstraňování cizorodých částic včetně některých patogenních mikroorganizmů a urychluje hojení ran. Působením rizikových faktorů aterosklerózy se tento ochranný účinek mění v účinek prozánětlivý a proaterogenní. Přehledný článek předkládá nové nálezy na podporu tzv. „Mohučské hypotézy“, podle níž ochranné působení CRP na počátku aterosklerotického procesu spočívá v řídícím vlivu CRP na aktivaci komplementu, kterou zahajují enzymaticky remodelované lipoproteiny o nízké hustotě. V dalším průběhu onemocnění je už působení CRP jasně proaterogenní, od progrese prvních morfologických změn tepenné stěny po rozvoj náhlých cévních příhod.
C-reactive protein can be viewed as a basic marker of activity of the inflammatory response, which modulates the development and the progression of atherosclerosis including its life-threatening complications. At the same time, C-reactive protein represents an active partaker or mediator of this same inflammatory reaction. However, at the very beginning of atherosclerotic disease, C-reactive protein exerts a clear-cut antiatherogenic activity. The two aspects of CRP’s function, i.e. both the pro-inflammatory and the anti-inflammatory one, respectively, stem from CRP’s extent of co-operation with the complement system. From the evolutional point of view, the anti-inflammatory activity of CRP is the primary one, in that it sets stage for the host to remove foreign particles and to accelerate wound healing. The influence of well-known atherogenic risk factors converts the originally beneficial influence of CRP into proinflammatory and pro-atherogenic effects. This review article presents new conclusions from the „Mainz hypothesis“. It shows that the primary protective action of CRP resides in its regulatory influence on the extent of activation of the complement system after the latter has been triggered by enzymatically remodeled low-density lipoproteins. In further course of atherosclerotic disease, C-reactive protein exhibits a full-blown proinflammatory activity. It can result in the progression of the primary morphologic lesions up to the development of sudden vascular events.
- MeSH
- aktivace komplementu fyziologie MeSH
- arterioskleróza patofyziologie MeSH
- C-reaktivní protein fyziologie MeSH
- enzymy fyziologie chemie MeSH
- lidé MeSH
- lipoproteiny LDL fyziologie klasifikace krev MeSH
- metaloproteasy fyziologie MeSH
- oxidační stres MeSH
- přehledová literatura jako téma MeSH
- proteasy fyziologie MeSH
- Check Tag
- lidé MeSH
1st ed. 309 s. : il.
- Konspekt
- Obecná genetika. Obecná cytogenetika. Evoluce
- NLK Obory
- genetika, lékařská genetika
Many aspects of protein function regulation require specific protein-protein interactions to carry out the exact biochemical and cellular functions. The highly conserved members of the 14-3-3 protein family mediate such interactions and through binding to hundreds of other proteins provide multitude of regulatory functions, thus playing key roles in many cellular processes. The 14-3-3 protein binding can affect the function of the target protein in many ways including the modulation of its enzyme activity, its subcellular localization, its structure and stability, or its molecular interactions. In this minireview, we focus on mechanisms of the 14-3-3 protein-dependent regulation of three important 14-3-3 binding partners: yeast neutral trehalase Nth1, regulator of G-protein signaling 3 (RGS3), and phosducin.
- MeSH
- DNA-glykosylasy chemie ultrastruktura MeSH
- DNA-lyasa (apurinová nebo apyrimidinová) chemie ultrastruktura MeSH
- fosfoproteiny chemie ultrastruktura MeSH
- konformace proteinů MeSH
- lidé MeSH
- molekulární sekvence - údaje MeSH
- multienzymové komplexy chemie ultrastruktura MeSH
- oční proteiny chemie ultrastruktura MeSH
- proteiny 14-3-3 chemie ultrastruktura MeSH
- proteiny RGS chemie ultrastruktura MeSH
- proteiny vázající GTP - regulátory chemie ultrastruktura MeSH
- Schizosaccharomyces pombe - proteiny chemie ultrastruktura MeSH
- sekvence aminokyselin MeSH
- vazba proteinů MeSH
- vazebná místa MeSH
- vztahy mezi strukturou a aktivitou MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
Since it has been demonstrated that soy diet can improve endothelial function, in the present study we evaluated the effect of dietary substitution of 25 g of animal proteins with soy proteins on endothelial dysfunction in renal transplant patients. METHODS: In 20 renal transplant patients (55 +/- 11 years, serum creatinine 1.7 +/- 0.6 mg/dl), brachial artery flow mediated dilation (FMD) and endothelium-independent vasodilation (sublingual nitroglycerine, 25 microg) were measured at baseline, after 5 weeks of a soy diet and finally after 5 weeks of soy wash-out. Changes in plasma lipids, markers of oxidative stress (lipid peroxides, LOOH) and inflammation (C-reactive protein), isoflavones (genistein and daidzein), asymmetric dimethyl arginine (ADMA) and L-arginine were also evaluated. RESULTS: At baseline, patients showed a significantly lower FMD as compared with age-matched healthy subjects (3.2 +/- 1.8 vs 6.3 +/- 1.9, respectively; P < 0.001), while response to nitroglycerine was similar. After soy diet, actual protein intake was not changed, cholesterol and lipid peroxides were significantly reduced, and isoflavones were detectable in plasma. Soy diet was associated with a significant improvement in FMD (4.4 +/- 2.0; P = 0.003 vs baseline), while response to nitroglycerine was unchanged. Improvement in FMD was related to L-arginine/ADMA ratio changes, but no significant relation was found to changes in cholesterol, lipid peroxides or genistein and daidzein plasma concentrations. After 5 weeks of soy diet discontinuation, FMD (3.3 +/- 1.7%) returned to baseline values and isoflavones were no longer detectable in plasma. CONCLUSIONS: A soy protein diet for 5 weeks improves endothelial function in renal transplant patients. This effect seems to be strictly dependent on soy intake as it disappears after soy withdrawal and is mediated by an increase in the L-arginine/ADMA ratio, independently of change in lipid profile, oxidative stress or isoflavones.
- MeSH
- C-reaktivní protein metabolismus MeSH
- cévní endotel embryologie metabolismus MeSH
- dieta MeSH
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- nemoci cév dietoterapie MeSH
- nemoci ledvin metabolismus MeSH
- oxidační stres MeSH
- peroxidace lipidů MeSH
- proteiny ze sójových bobů metabolismus MeSH
- senioři MeSH
- transplantace ledvin metody MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
The human gene that encodes XRCC1 was cloned nearly thirty years ago but experimental analysis of this fascinating protein is still unveiling new insights into the DNA damage response. XRCC1 is a molecular scaffold protein that interacts with multiple enzymatic components of DNA single-strand break repair (SSBR) including DNA kinase, DNA phosphatase, DNA polymerase, DNA deadenylase, and DNA ligase activities that collectively are capable of accelerating the repair of a broad range of DNA single-strand breaks (SSBs). Arguably the most exciting aspect of XRCC1 function that has emerged in the last few years is its intimate relationship with PARP1 activity and critical role in preventing hereditary neurodegenerative disease. Here, I provide an update on our current understanding of XRCC1, and on the impact of hereditary mutations in this protein and its protein partners on human disease.
- MeSH
- DNA metabolismus MeSH
- dvouřetězcové zlomy DNA MeSH
- jednořetězcové zlomy DNA MeSH
- lidé MeSH
- oprava DNA * MeSH
- protein XRCC1 metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
