末端プロペプチドとは何ですか？
Terminal Propeptide 末端プロペプチド - Two serum markers of either bone formation—N-terminal propeptide of type I procollagen (P1NP) or bone resorption—C-terminal telopeptide of type I collagen (CTX-I)—were analyzed in a cohort of patients with psoriasis vulgaris. [1] Sequence elements in the ZPD and the carboxy-terminal propeptide of ZP1–4 regulate secretion and assembly of nascent ZP proteins. [2] Correlation and multivariate regression analysis of relationships between the relative abundance of intestinal bacteria and the concentration of the procollagen type I carboxy-terminal propeptide (PICP) and N-terminal propeptide of procollagen type III (PIIINP) was carried out. [3] Results Age, appetite, serum alanine aminotransferase activity, body condition, serum creatinine concentration, murmur intensity, and plasma N‐terminal propeptide of B‐type natriuretic peptide (NT‐proBNP) concentration were independently associated with the likelihood of being stage B2. [4] By studying the mechanism underlying OA cartilage injury and changes in the concentrations of the biomarkers procollagen type II carboxy-terminal propeptide (PIICP), collagen type-II C-telopeptide fragments (CTX-II), and type II collagen cleavage neoepitope (C2C) during pathogenesis, the present study established a theoretical basis for the evaluation and early diagnosis of OA. [5] We compared BTMs [alkaline phosphatase (ALP); osteocalcin (OC); procollagen 1 intact N-terminal propeptide (P1NP)], serum calcium, renal function, radiological findings, and functional outcomes (Harris hip score and UCLA activity score) from baseline to 5 years post-THA in 49 patients, and periprosthetic BMD of the seven Gruen zones in 19 patients. [6] Significant differences in peptide yields, observed within collagen I, II and V α-chains (COL1A2, COL2A1, COL5A1), were located within their triple helical regions and/or cleaved Cterminal propeptides, indicating potential accumulation of damage and impaired maintenance in ageing. [7] blood biomarkers (amino-terminal propeptide of procollagen type III (PIIINP) and carboxy-terminal propeptide of procollagen type I (PICP)), iii. [8] BACKGROUND After myocardial infarction (MI) complicated by heart failure (HF), eplerenone reduced serum concentrations of amino-terminal propeptide of type III collagen (PIIINP) and carboxy-terminal propeptide of type I collagen (PICP). [9] Intracellular procollagen folding begins at the protein’s C-terminal propeptide (C-Pro) domain, which initiates triple-helix assembly and defines the composition and chain register of fibrillar collagen trimers. [10] In the RM-ANOVA analysis, anti-TNF treatment together with baseline osteocalcin, procollagen 1 N-terminal propeptide (P1NP) or vitamin D3 levels determined one-year changes in IMT (p < 0. [11] Results The predicting accuracy rate of final model was above 88%, with feature combination of sex, age, BMI (body mass index), TP1NP (total procollagen I N-terminal propeptide) and OSTEOC (osteocalcin). [12] Serum levels of hyaluronan (HA), cartilage oligomeric matrix protein (COMP), aggrecan chondroitin sulphate 846 (CS846), glycoprotein YKL-40, human procollagen II N-terminal propeptide (PIINP), human type IIA collagen N-propeptide (PIIANP), and collagen type II cleavage (C2C) were measured by sandwich enzyme-linked immune-sorbent assay (ELISA). [13] During continuous collagen synthesis propeptides, like procollagen type I carboxy-terminal propeptide (PICP) and during collagen breakdown, C-terminal telopeptide collagen type I (ICTP), are released into the circulation. [14] The in silico analysis showed that DgeKer is composed of signal peptide, N-terminal propeptide, mature domain, and C-terminal extension. [15] N-terminal propeptide of type I collagen (PINP) was analysed as a marker of bone formation. [16] This surprising result is achieved by simply deleting from the input sequence a stretch of residues that correspond to a polymerization‐inhibiting C‐terminal propeptide. [17] A second ECG was urgently performed, as a result of which an increase in the ST segment in III, aVF was established, as well as a study of the concentration of cardiomarkers: highly sensitive troponin I, N-terminal propeptide of natriuretic hormone, creatine phosphokinase MB, myoglobin, the dynamics of changes in the level of which indicated the development of acute coronary syndrome. [18] Changes from baseline in serum C-terminal telopeptide of type I collagen (CTX), procollagen type I N-terminal propeptide (P1NP), and lumbar spine (LS) and total hip (TH) BMD were evaluated. [19] Comparison of baseline factors showed that patients without APRs in the ZOL group had a significantly higher neutrophil/lymphocyte ratio, lower serum levels of procollagen type I N-terminal propeptide, older age, and higher likelihood of prior bisphosphonate use vs patients with APRs. [20] Present results further elucidate the inheritance pattern of HESX1 variants and recommend assessing the clinical impact of variants located in C-terminal propeptide of COL1A1 gene for their potential association with rare recessive and early onset forms of osteoporosis. [21] Homeostasis model assessment of insulin resistance (HOMA-IR) and β-cell dysfunction (HOMA-%β) were applied to elucidate the nexus between β-C-terminal telopeptide (β-CTX), intact N-terminal propeptide of type I collagen (P1NP) and osteocalcin (OC). [22] Peripheral venous blood samples from 108 patients and healthy subjects underwent total hip replacement were collected to detect the levels of plasma biomarkers procollagen type I carboxy-terminal propeptide (PICP), N-telopeptide cross-links of type I collagen (NTX), osteoprotegerin (OPG), TNGα, receptor activator of NF-kappaB ligand (RANKL), and IL-1β. [23] Ten ECM biomarkers were measured from plasma in 140 AMI patients: MMP-2, -3, -8, -9, periostin, procollagen I N-Terminal propeptide, osteopontin, TGF-β1, TIMP-1 and -4. [24] Serum levels of hypoxia-inducible factor 1-alpha (HIF-1α), endogenous erythropoietin (eEPO), N-terminal propeptide of type B natriuretic hormone (NT-proBNP), cystatin C were assessed. [25] Activation of the endopeptidases requires removal of an inhibitory N-terminal propeptide. [26] Serum markers of bone turnover (osteocalcin (OC), N-terminal propeptide of type-I procollagen (PINP), reflecting bone formation, and carboxyterminal collagen I crosslinks (CTX-I), reflecting bone resorption) and BMD (by DXA) were measured before the intervention and at follow-up. [27] Health records were screened for pain scores, side effects, and bone turnover markers (BTMs) (calcium, alkaline phosphatase [ALP], procollagen 1 N‐terminal propeptide [P1NP], and β‐crosslaps [B‐CTX, also termed β–C‐terminal telopeptide]) during treatment, and for BTMs and clinical rebound effects after withdrawal. [28] After the initiation of oral bisphosphonates, a resorption marker such as C-telopeptide of type I collagen (CTX) reaches a nadir ~70% below baseline at 1 to 4 weeks, and a formation marker such as N-terminal propeptide of type I procollagen (PINP) reaches its nadir (~60% below baseline) at about 12 weeks. [29] Echocardiography, serum procollagen I C-terminal propeptide (PICP) procollagen III N-terminal propeptide (PIIINP) and C telopeptide type I (CTX-I) were evaluated at baseline and 3, 6 and 9 weeks after initial DOX administration for all surviving rats. [30] Rats were then euthanized and the aortas and tibias were dissected for histological examination and estimation of MMP-9, N-terminal propeptide of type I procollagen (PINP), C-terminal telopeptide of type I collagen (CTX) and NF-kB expression. [31] We detected the concentrations of procollagen type-I C-terminal propeptide (PICP), procollagen type-III N-terminal propeptide (PIIINP), and angiotensin II (AngII) in rat serum. [32] cycling (low-impact), at the same moderate-to-vigorous exercise intensity, on markers of bone formation (N-terminal propeptide of type I collagen, PINP) and bone resorption (C-telopeptide of type I collagen, CTX-1), a non-collagenous bone remodeling marker (osteocalcin), as well as bone-modulating factors, including parathyroid hormone (PTH), irisin (myokine) and sclerostin (osteokine). [33] In the monitoring group, serum BTMs (C-telopeptide of type I collagen (CTX-I), N-terminal propeptide of type I procollagen (PINP), and 25(OH)D) were assessed preoperatively and repeated postoperatively; alendronate was withdrawn when CTX-I and PINP reached the reference interval; and calcitriol and calcium were withdrawn when 25(OH)D reached the reference interval. [34] MAIN OUTCOME MEASURES The study was designed to test the impact of 3OHB on PTH, calcium-phosphate, C-terminal Telopeptide (CTX), and Procollagen I N-terminal Propeptide (PINP). [35] On the 12th day, the serum concentration of procollagen type I carboxy-terminal propeptide (PICP), N-terminal propeptide of procollagen type III (PIIINP), and galectin-3 was determined, as well as echocardiography was performed to assess left ventricular DF. [36] We measured total, free, and bioavailable testosterone, estradiol, and sex-hormone-binding globulin (sex hormones), as well as parathyroid hormone, osteocalcin, carboxy terminal collagen crosslinks, and N-terminal propeptide of type I procollagen (markers of bone turnover). [37] The newly generated splice acceptor in exon 50 is much more accessible than the wild-type splice-site between the junction of exon 49 and 50, and results in an in-frame deletion of 24 amino acids of the C-terminal propeptide. [38] The levels of N-terminal propeptide of type I collagen (PINP) and C-terminal telopeptide of type I collagen (CTx-I) in rat serum were evaluated by ELISA assays. [39] Aim: Having in mind the pathological collagen type I turnover in preeclampisa, the aim of the present study was to determine the levels of N-terminal propeptide of collagen type I (PINP), C-terminal propeptide of collagen type I (PICP): both markers of collagen type I synthesis and levels of matrix metalloproteinase-1 (MMP-1): marker of collagen type I degradation in sera of women with early-onset preeclampsia. [40] The following parameters were determined in the blood by the enzyme immunoassay: renin, aldosterone, n-terminal propeptide of natriuretic hormone (NТ-рroВNР). [41] Study outcomes were the changes in LSBMD, LSBMD z-scores, and bone metabolism-related biomarkers (25-hydoxyvitamin D[25OHD], intact parathyroid hormone[iPTH], C-terminal telopeptide[CTX], procollagen type I amino-terminal propeptide[PINP]) from baseline to week48. [42] One bone marker, N-terminal propeptide of type I procollagen (PINP), significantly decreased from 146. [43] Serum biomarkers of bone formation, procollagen 1 intact N-terminal propeptide (P1NP), and resorption, c-terminal telopeptide of type I collagen (CTX-1) were assessed. [44] Serum N-terminal propeptide of type I collagen (P1NP), cross-linked N-telopeptide of type I collagen (NTX), and parathyroid hormone (PTH) levels were measured and dual-energy X-ray absorptiometry (DXA) scans were taken pre- and post-intervention. [45] AIS showed significantly lower BMD, circulating WNT16 level, and elevated serum level of type I procollagen N-terminal propeptide. [46] There was no significant change in N-terminal propeptide of procollagen type I (P1NP), osteocalcin, or C-telopeptide of type I collagen (CTX) from baseline to day 11 (all p ≥0. [47] Serum levels of aminoterminal propeptide of type I collagen (P1NP), C terminal telopeptide of type I collagen (CTX), alkaline phosphatase (AP), 25hydroxyvitamin D (25-OHD), parathyroid hormone (PTH), were measured at 3 time points: T0 (before beginning HBOT), T1 (at the end of HBOT) and T2 (6 months after HBOT). [48] Fasting plasma levels of C-terminal telopeptides of type I collagen, a marker of bone resorption, and amino-terminal propeptide of type I procollagen, a marker of bone formation, were unchanged by exenatide compared with placebo after 26 weeks. [49]尋常性乾癬患者のコホートで、骨形成の2つの血清マーカー（I型プロコラーゲンのN末端プロペプチド（P1NP）または骨吸収）の2つの血清マーカー（I型コラーゲンのC末端テロペプチド（CTX-I））を分析しました。 [1] ZPDの配列要素とZP1–4のカルボキシ末端プロペプチドは、新生ZPタンパク質の分泌と集合を調節します。 [2] 腸内細菌の相対存在量とプロコラーゲンI型カルボキシ末端プロペプチド（PICP）およびプロコラーゲンIII型のN末端プロペプチド（PIIINP）の濃度との関係の相関および多変量回帰分析を実施しました。 [3] 結果年齢、食欲、血清アラニンアミノトランスフェラーゼ活性、体調、血清クレアチニン濃度、雑音強度、およびB型ナトリウム利尿ペプチド（NT-proBNP）濃度の血漿N末端プロペプチドは、B2期である可能性と独立して関連していた。 [4] 変形性関節症の軟骨損傷の根底にあるメカニズムと、バイオマーカーであるプロコラーゲンタイプIIカルボキシ末端プロペプチド（PIICP）、コラーゲンタイプII C-テロペプチドフラグメント（CTX-II）、およびタイプIIコラーゲン切断ネオエピトープ（C2C）の濃度の変化を研究することによって病因の間に、本研究はOAの評価と早期診断のための理論的基礎を確立しました。 [5] BTM [アルカリホスファターゼ（ALP）]を比較しました。オステオカルシン（OC）;プロコラーゲン1インタクトN末端プロペプチド（P1NP）]、血清カルシウム、腎機能、放射線所見、およびベースラインからTHA後5年までの49人の患者の機能的転帰（ハリスヒップスコアおよびUCLA活性スコア）、および人工関節周囲BMD 19人の患者の7つのGruenゾーン。 [6] コラーゲンI、IIおよびVα鎖（COL1A2、COL2A1、COL5A1）内で観察されたペプチド収量の有意差は、それらの三重らせん領域および/または切断されたC末端プロペプチド内に位置し、損傷の潜在的な蓄積および老化における障害のある維持を示しています。 [7] 血液バイオマーカー（プロコラーゲンタイプIIIのアミノ末端プロペプチド（PIIINP）およびプロコラーゲンタイプIのカルボキシ末端プロペプチド（PICP））、iii。 [8] バックグラウンド 心不全（HF）を合併した心筋梗塞（MI）の後、エプレレノンは、III型コラーゲンのアミノ末端プロペプチド（PIIINP）およびI型コラーゲンのカルボキシ末端プロペプチド（PICP）の血清濃度を低下させました。 [9] 細胞内プロコラーゲンフォールディングは、タンパク質のC末端プロペプチド（C-Pro）ドメインで始まります。これにより、三重らせんの組み立てが開始され、線維状コラーゲン三量体の組成と鎖の見当が定義されます。 [10] RM-ANOVA分析では、ベースラインのオステオカルシン、プロコラーゲン1のN末端プロペプチド（P1NP）、またはビタミンD3レベルと併用した抗TNF治療により、IMTの1年間の変化が決定されました（p<0。 [11] 結果 最終モデルの予測正解率は88％を超え、性別、年齢、BMI（ボディマス指数）、TP1NP（総プロコラーゲンIN末端プロペプチド）およびOSTEOC（オステオカルシン）の特徴の組み合わせがありました。 [12] ヒアルロン酸（HA）、軟骨オリゴマー基質タンパク質（COMP）、アグリカンコンドロイチン硫酸塩846（CS846）、糖タンパク質YKL-40、ヒトプロコラーゲンII N末端プロペプチド（PIINP）、ヒトIIA型コラーゲンN-プロペプチド（PIIANP）の血清レベル、およびコラーゲンタイプII切断（C2C）は、サンドイッチ酵素結合免疫吸着測定法（ELISA）によって測定されました。 [13] プロコラーゲンI型カルボキシ末端プロペプチド（PICP）のような連続的なコラーゲン合成プロペプチドの間、およびコラーゲン分解の間、C末端テロペプチドコラーゲンI型（ICTP）は循環に放出されます。 [14] インシリコ分析は、DgeKerがシグナルペプチド、N末端プロペプチド、成熟ドメイン、およびC末端伸長で構成されていることを示しました。 [15] I型コラーゲンのN末端プロペプチド（PINP）を骨形成のマーカーとして分析しました。 [16] この驚くべき結果は、重合阻害C末端プロペプチドに対応する一連の残基を入力配列から単に削除することによって達成されます。 [17] 2番目のECGが緊急に実行され、その結果、IIIのSTセグメントの増加、aVFが確立され、心臓マーカーの濃度の研究も行われました：高感度トロポニンI、ナトリウム利尿ホルモンのN末端プロペプチド、クレアチンホスホキナーゼMB、ミオグロビン、そのレベルの変化のダイナミクスは、急性冠症候群の発症を示しました。 [18] I型コラーゲン（CTX）の血清C末端テロペプチド、プロコラーゲンI型N末端プロペプチド（P1NP）、腰椎（LS）および総股関節（TH）BMDのベースラインからの変化を評価しました。 [19] ベースライン要因の比較は、ZOLグループのAPRのない患者は、APRのある患者と比較して、有意に高い好中球/リンパ球比、プロコラーゲンI型N末端プロペプチドの低い血清レベル、高齢、および以前のビスホスホネート使用の可能性が高いことを示しました。 [20] 現在の結果は、HESX1変異体の遺伝パターンをさらに解明し、COL1A1遺伝子のC末端プロペプチドに位置する変異体の臨床的影響を、まれな劣性および早期発症型の骨粗鬆症との潜在的な関連性について評価することを推奨しています。 [21]