Seracare心肌磷脂IgA（Cardiolipin IgA）
| 型 號： | 美國 |
| 報 價： |  |
美國SeracareSeracare心肌磷脂IgA（Cardiolipin IgA） 陽性質(zhì)控品對照品 需要了解更多Seracare產(chǎn)品可以咨詢我們，本產(chǎn)品由廣州健侖生物科技有限公司提供
- 產(chǎn)品描述
美國Seracare心肌磷脂IgA（Cardiolipin IgA）
廣州健侖生物科技有限公司
廣州健侖長期供應(yīng)各種生物原料，主要代理品牌：美國Seracare、西班牙Certest、美國Fuller等等。
主要產(chǎn)品包括各種標準品、陽性對照品、單克隆抗原抗體。
其中常見的有：弓形蟲病、西尼羅河病毒、類風(fēng)濕因子、瘧疾、麻疹、萊姆病、百日咳桿菌、大腸桿菌、鼠傷寒沙門氏菌、李斯特菌等陽性對照品。
美國Seracare心肌磷脂IgA（Cardiolipin IgA）
我司還提供其它進口或國產(chǎn)試劑盒：登革熱、瘧疾、流感、A鏈球菌、合胞病毒、腮病毒、乙腦、寨卡、黃熱病、基孔肯雅熱、克錐蟲病、違禁品濫用、肺炎球菌、軍團菌、化妝品檢測、食品安全檢測等試劑盒以及日本生研細菌分型診斷血清、德國SiFin診斷血清、丹麥SSI診斷血清等產(chǎn)品。
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【Seracare產(chǎn)品介紹】
編號 | 英文名稱 | 中文名稱 |
JL-FA-01 | Amebiasis (AME) | 阿米巴病 |
JL-FA-02 | Allergens, Rast scores | 過敏原，放射性過敏原吸收實驗。指對特定的人群引起免疫反應(yīng)或者過敏反應(yīng)的食品中的蛋白質(zhì) |
JL-FA-03 | Allergens, Rast scores negative | 過敏原，放射性過敏原吸收實驗陰性 |
JL-FA-04 | Anti-cyclic citrullinated peptide Antibody (CCP) Arthritis | 抗環(huán)瓜氨酸肽抗體 |
JL-FA-05 | ASCA Saccharomyces Cerevi | 人抗釀酒酵母抗體（ASCA） |
JL-FA-06 | Aspergillis | 麴菌病 |
JL-FA-07 | Beta 2 Glycoprotein | β2糖蛋白 |
JL-FA-08 | Beta 2 Glycoprotein IgM | β2糖蛋白 IGM |
JL-FA-09 | Bordela Pertussis | 百日咳桿菌 |
JL-FA-10 | Bordela Pertussis IgM | 百日咳桿菌 IGM |
JL-FA-11 | C-ANCA | C-抗中性粒細胞胞漿抗體（ANCA) |
JL-FA-12 | Cardiolipin | 心肌磷脂 |
JL-FA-13 | Cardiolipin IgA | 心肌磷脂 IGA |
JL-FA-14 | Cardiolipin IgG | 心肌磷脂 IGG |
JL-FA-15 | Cardiolipin IgM | 心肌磷脂 IGM |
JL-FA-16 | Cerebral Spinal Fluid | 腦脊髓液 |
JL-FA-17 | Chagas | 恰加斯病/南美錐蟲 |
JL-FA-18 | Chlamydia | 衣原體 |
JL-FA-19 | Chlamydia IgA | 衣原體IGA |
JL-FA-20 | Chlamydia IgG | 衣原體IGG |
JL-FA-21 | Chlamydia IgM | 衣原體IGM |
JL-FA-22 | Chlamydia Neg | 衣原體陰性 |
JL-FA-23 | Clotting Factor C3 | 凝固因子C3 |
JL-FA-24 | Clotting Factor C4 | 凝固因子C4 |
JL-FA-25 | Coccidiodes | 球孢菌 |
JL-FA-26 | Cytomegalovirus (CMV) Neg | 巨細胞病毒抗體陰性 |
JL-FA-27 | CMV IgG | 巨細胞病毒 IGG陽性 |
JL-FA-28 | CMV IgM VCA | 巨細胞病毒 IGM 陽性 |
JL-FA-29 | C-Reactive Protein (CRP) | C-反應(yīng)蛋白質(zhì) |
JL-FA-30 | Dengue Fever | 登革熱 |
JL-FA-31 | Dengue Fever IgM | 登革熱 IGM |
JL-FA-32 | DS (Double Stranded) DNA | 雙鏈脫氧核糖核酸 |
JL-FA-33 | EBNA (Epstein-Barr nuclear antigen) IgG | EB病毒核抗原 IGG |
JL-FA-34 | EBNA (Epstein-Barr nuclear antigen) IgM | EB病毒核抗原 IGM |
JL-FA-35 | Epstein Barr Virus (EBV) Negative Plasma | EB病毒陰性血漿 |
JL-FA-36 | Epstein Barr Virus (EBV) EA IgM | EB病毒早期抗原 IGM |
JL-FA-37 | Epstein Barr Virus (EBV) VCA IgM | EB病毒殼蛋白 IGM |
JL-FA-38 | Epstein Barr Virus (EBV) EA IgG | EB病毒早期抗原 IGG |
JL-FA-39 | EMA (Endomysial Antibodies) | 肌內(nèi)膜 |
JL-FA-40 | Gliadin | 麩蛋白,麥醇溶蛋白,麥膠蛋白 |
JL-FA-41 | Gliadin IgG | 麥醇溶蛋白 IGG |
JL-FA-42 | Gliadin IgA | 麥醇溶蛋白 IGA |
JL-FA-43 | Glomerular Basement Membrane (GBMA) | 腎小球基底膜病 |
JL-FA-44 | Helicobacter pylori IgA | 幽門螺旋桿菌IGA |
JL-FA-45 | Helicobacter pylori IgG | 幽門螺旋桿菌IGG |
JL-FA-46 | Helicobacter pylori IgM | 幽門螺旋桿菌IGM |
JL-FA-47 | Helicobacter pylori Negative | 幽門螺旋桿菌陰性 |
JL-FA-48 | Helicobacter pylori Positive Plasma | 幽門螺旋桿菌陰性血漿 |
JL-FA-49 | Hepatitis A Virus (HAV) Pos. Plasma | 甲型肝炎病毒陽性血漿 |
JL-FA-50 | Hepatitis A Virus (HAV) IgM | 甲型肝炎病毒IGM |
JL-FA-51 | Hepatitis B Core (HBc) IgG | 乙型肝炎病毒核心 IGG |
JL-FA-52 | Hepatitis B Core (HBc) IgM | 乙型肝炎病毒核心 IGM |
JL-FA-53 | Anti Hbe (Antibody to HBV antigen) | 乙肝抗體 |
JL-FA-54 | Hepatitis Delta Virus | 丁型肝炎病毒 |
JL-FA-55 | HBeAg (HBV e antigen) | 乙肝 E抗原 |
JL-FA-56 | anti-HBs (HBV surface antibody) | 乙肝表面抗體 |
JL-FA-57 | Hepatitis B (HBsAg) "Chronic" | 乙型肝炎（乙肝表面抗原）“慢性病 |
JL-FA-58 | HBsAg (HBV surface antigen) Serum | 乙肝表面抗原血清 |
JL-FA-59 | HBsAg (AD) | 乙肝表面抗原（AD） |
JL-FA-60 | HBsAg (AY) | 乙肝表面抗原（AY） |
JL-FA-61 | HBV Positive Plasma | 乙肝陽性血漿 |
JL-FA-62 | HBV DNA Plasma | 乙肝DNA血漿 |
JL-FA-63 | HBV DNA Serum | 乙肝DNA血清 |
JL-FA-64 | HBV DNA type A | A型 乙肝DNA |
JL-FA-65 | HBV DNA type B | B型 乙肝DNA |
JL-FA-66 | HBV DNA type C | C型 乙肝DNA |
JL-FA-67 | HBV DNA type D | D型 乙肝DNA |
JL-FA-68 | HBV DNA type E | E型 乙肝DNA |
JL-FA-69 | HBV DNA type F | F型 乙肝DNA |
JL-FA-70 | HBV Antibody HCV Antibody Plasma CO-INFECTED | 乙肝和丙肝聯(lián)合感染血漿 |
JL-FA-71 | HCV (Hepatitis C Virus) Antibody | 丙型肝炎抗體 |
JL-FA-72 | HCV Core Antigen Positive | 丙肝核心抗原 陽性 |
JL-FA-73 | HCV RNA PLASMA Genotype 1 | 基因1型丙肝RNA 血漿 |
JL-FA-74 | HCV RNA PLASMA Genotype 2 | 基因2型丙肝RNA 血漿 |
JL-FA-75 | HCV RNA PLASMA Genotype 3 | 基因3型丙肝RNA 血漿 |
JL-FA-76 | HCV RNA PLASMA Genotype 4 | 基因4型丙肝RNA 血漿 |
JL-FA-77 | HCV RNA PLASMA Genotype 5 | 基因5型丙肝RNA 血漿 |
JL-FA-78 | HCV RNA PLASMA Genotype 6 | 基因6型丙肝RNA 血漿 |
JL-FA-79 | HCV Riba single band | 丙肝免疫印跡單波段 |
JL-FA-80 | HCV RIBA Pos. (multiple bands) | 丙肝免疫印跡陽性多波段 |
JL-FA-81 | HCV Negative | 丙肝陰性 |
JL-FA-82 | HCV RNA Pos (quantitative) | 丙肝RNA陽性（定量） |
JL-FA-83 | Hepatitis E | 戊型肝炎 |
JL-FA-84 | Herpes Simplex Virus (HSV)1/2 Positive Plasma | 單純性皰疹病毒1/2陽性血漿 |
JL-FA-85 | Herpes Simplex Virus (HSV) 1 Negative Plasma | 單純性皰疹病毒1 陰性血漿 |
JL-FA-86 | Herpes Simplex Virus (HSV) 1 IgG | 單純性皰疹病毒1 IGG |
JL-FA-87 | Herpes Simplex Virus (HSV 1) IgM | 單純性皰疹病毒1 IGM |
JL-FA-88 | Herpes Simplex Virus (HSV) 2 IgG | 單純性皰疹病毒2 IGG |
JL-FA-89 | Herpes Simplex Virus (HSV) 2 IgM | 單純性皰疹病毒2 IGG |
JL-FA-90 | Histone | 組蛋白 |
JL-FA-91 | Human Anti Mouse Ab (HAMA) | 人抗鼠抗體 |
JL-FA-92 | Human immunodeficiency virus (HIV) 1 Neg | HIV I 陰性 |
JL-FA-93 | anti Human immunodeficiency virus (HIV) 1 Plasma | 抗HIV I 血漿 |
JL-FA-94 | anti Human immunodeficiency virus (HIV) 1 Serum | 抗HIV I 血清 |
JL-FA-95 | anti Human immunodeficiency virus (HIV) 2 Western Blot Tested | 抗HIV 2 免疫印跡 |
JL-FA-96 | anti Human immunodeficiency virus (HIV) 1/2 2 HIV (+) | 抗HIV 1/2 2 HIV陽性 |
JL-FA-97 | Human immunodeficiency virus (HIV) Ag | HIV抗原 |
JL-FA-98 | HIV RNA (quantitative) Plasma | HIV RNA 定量血漿 |
JL-FA-99 | HIV RNA (quantitative) Serum | HIV RNA 定量血清 |
JL-FA-100 | HIV1 Subtype A | HIV1 亞型A |
JL-FA-101 | HIV1 Subtype B | HIV1 亞型B |
JL-FA-102 | HIV1 Subtype C | HIV1 亞型C |
JL-FA-103 | HIV1 Subtype D | HIV1 亞型D |
JL-FA-104 | HIV1 Subtype E | HIV1 亞型E |
JL-FA-105 | HIV1 Subtype F | HIV1 亞型F |
JL-FA-106 | HIV1 Subtype G | HIV1 亞型G |
JL-FA-107 | HIV1 Subtype H | HIV1 亞型H |
JL-FA-108 | HIV1 Subtype J | HIV1 亞型J |
JL-FA-109 | HIV1 Subtype K | HIV1 亞型K |
JL-FA-110 | HIV1 Group O | HIV1 亞型O |
JL-FA-111 | Human immunodeficiency virus (HIV) 2 Antibody Plasma | HIV 2 抗體血漿 |
JL-FA-112 | Human immunodeficiency virus (HIV) 2 Antibody Serum | HIV 2 抗體血清 |
JL-FA-113 | HPV (Human Papiloma Virus) Negative | 人乳狀瘤病毒HPV陰性 |
JL-FA-114 | HPV (Human Papiloma Virus) Positive | 人乳狀瘤病毒HPV陽性 |
JL-FA-115 | Human immunodeficiency virus (HIV) Antibody HCV Antibody Plasma COINFECTED | HIV 抗體 HCV |
JL-FA-116 | Human T-cell Lymphotropic Virus (HTLV) I/II | 人嗜T淋巴細胞病毒(HTLV) I/II |
JL-FA-117 | Human T-cell Lymphotropic Virus (HTLV) I | 人嗜T淋巴細胞病毒(HTLV) I |
JL-FA-118 | Human T-cell Lymphotropic Virus (HTLV) II | 人嗜T淋巴細胞病毒(HTLV) II |
JL-FA-119 | Jo-1 | 多發(fā)性肌炎抗原JO-1 |
JL-FA-120 | IgE < 5,000 Ku/L | IgE < 5,000 Ku/L |
JL-FA-121 | Legionella | 軍團桿菌屬 |
JL-FA-122 | Leptospira | 軍團桿菌屬 |
JL-FA-123 | Lyme Disease | 萊姆(氏)病:蜱傳播的全身性疾病,常在夏季發(fā)生 |
JL-FA-124 | Lyme IgG | 萊姆(氏)病 IGG |
JL-FA-125 | Lyme IgM | 萊姆(氏)病 IGM |
JL-FA-126 | Lyme Disease Neg | 萊姆(氏)病 陰性 |
JL-FA-127 | Malaria | 瘧疾 |
JL-FA-128 | Mononucleosis (infectious) | 單核細胞增多癥（有傳染性的） |
JL-FA-129 | Mononucleosis Negative | 單核細胞增多癥陰性 |
JL-FA-130 | Measles Negative | 麻疹 陰性 |
JL-FA-131 | Measles IgG | 麻疹 IGG |
JL-FA-132 | Measles IgM | 麻疹 IGM |
JL-FA-133 | Microsomal Anti-thyroid peroxidase antibody (TPO) Positive Plasma Standard Titer (typically 1,000-3,000 IU/mL) | 微粒體抗甲狀腺過氧化物酶抗體 |
JL-FA-134 | Microsomal Anti-thyroid peroxidase antibody (TPO) Negative Plasma | 微粒體抗甲狀腺過氧化物酶抗體 |
JL-FA-135 | Anti-mitochondrial antibody (AMA) | 抗線粒體抗體 |
JL-FA-136 | Multiple Sclerosis | 多發(fā)性硬化癥 |
JL-FA-137 | Mumps IgG | 流行性腮腺炎 IGG |
JL-FA-138 | Mumps Ab IgM | 流行性腮腺炎抗體 IGM |
JL-FA-139 | Mumps Antibody Negative Plasma | 流行性腮腺炎抗體陰性血漿 |
JL-FA-140 | Mumps Antibody Negative Serum | 流行性腮腺炎抗體陰性血清 |
JL-FA-141 | Myeloma Plasma | 骨髓瘤血漿 |
JL-FA-142 | Myeloma IgA | 骨髓瘤IGA |
JL-FA-143 | Myeloma IgE | 骨髓瘤IGE |
JL-FA-144 | Myeloma IgG | 骨髓瘤IGG |
JL-FA-145 | Myeloma IgM | 骨髓瘤IGM |
JL-FA-146 | Mycoplasma | 支原體 |
JL-FA-147 | Mycoplasma Negative | 支原體陰性 |
JL-FA-148 | Mycoplasma IgG | 支原體IGG |
JL-FA-149 | Mycoplasma IgM | 支原體IGM |
JL-FA-150 | Mycoplasma PCR | 支原體PCR |
JL-FA-151 | Normal Human Plasma | 正常人血漿 |
JL-FA-152 | Normal Human Serum | 正常人血清 |
JL-FA-153 | Nuclear Antibody Centromere | 核抗體著絲粒 |
JL-FA-154 | Nuclear Antibody, Speckled ANA | 核抗體，斑點抗核抗體 |
JL-FA-155 | Nuclear Antibody, Nucleolar ANA | 核抗體,核仁抗核抗體 |
JL-FA-156 | Nuclear Antibody, Homogeneous ANA | 核抗體，同質(zhì)抗核抗體 |
JL-FA-157 | Nuclear Antiobody, Speckled. (ANA) Negative | 核抗體，斑點。抗核抗體陰性 |
JL-FA-158 | P-ANCA (associated neutrophil cytoplasmic antibodies) | 相關(guān)的嗜中性粒細胞胞漿抗體 |
JL-FA-159 | Parietal Cell Antibody (PCA) | 胃)壁細胞抗體 |
JL-FA-160 | Parvo positive plasma | 細小病毒陽性血漿 |
JL-FA-161 | Parvo IgM | 細小病毒 IGM |
JL-FA-162 | Parvo IgG | 細小病毒 IGG |
JL-FA-163 | Parvo Negative Plasma | 細小病毒陰性血漿 |
JL-FA-164 | Parvo DNA positive | 細小病毒 DNA 陽性 |
JL-FA-165 | Phospholipid Positive Plasma | 磷脂陽性血漿 |
JL-FA-166 | Prothrombin | 凝血酶原,凝血因子 |
JL-FA-167 | Rheumatoid Factor (RF) <1000 IU/mL | 類風(fēng)濕因子<1000 IU/mL |
JL-FA-168 | Rheumatoid Factor (RF) 1001-2000 IU/mL | 類風(fēng)濕因子1001-2000 IU/mL |
JL-FA-169 | Rheumatoid Factor (RF) 2001-4000 IU/mL | 類風(fēng)濕因子 2001-4000 IU/mL |
JL-FA-170 | Rheumatoid Factor (RF) 4001-5000 IU/mL | 類風(fēng)濕因子 4001-5000 IU/mL |
JL-FA-171 | Rheumatoid Factor (RF) >5000 IU/mL | 類風(fēng)濕因子>5000 IU/mL |
JL-FA-172 | Ribonucleoprotein (RNP) Positive | 核糖核蛋白陽性 |
JL-FA-173 | Rubella Chimeric | 風(fēng)疹 |
JL-FA-174 | Rubella Negative | 風(fēng)疹陰性 |
JL-FA-175 | Rubella IgG | 風(fēng)疹I(lǐng)GG |
JL-FA-176 | Rubella IgM | 風(fēng)疹I(lǐng)GM |
JL-FA-177 | Rubeola Negative Plasma | 風(fēng)疹陰性血漿 |
JL-FA-178 | Rubeola IgG | 風(fēng)疹I(lǐng)GG |
JL-FA-179 | Scleroderma (Scl-70) Pos | 膠原沉著病,硬皮病,硬皮癥 陽性 |
JL-FA-180 | Scleroderma (Scl-70) Negative | 硬皮病陰性 |
JL-FA-181 | Sickle Cell Fresh Whole Blood | 鐮刀形紅細胞新鮮全血 |
JL-FA-182 | Smith (SM) | 抗Smith抗體陽性血清（SLE的特征性抗體） |
JL-FA-183 | SMITH RNP | 抗RNP抗體陽性血清（SLE的特征性抗體） |
JL-FA-184 | Smooth Muscle (ASMA) | 抗平滑肌抗體陽性血清 |
JL-FA-185 | Sjogren syndrome antigen A (SSA) Positive | 舍格倫綜合征或干燥綜合征抗原A 陽性 |
JL-FA-186 | Sjogren syndrome antigen B (SSB) Positive | 舍格倫綜合征抗原B 陽性 |
JL-FA-187 | Sjogren syndrome antigen B (SSB) Negative | 舍格倫綜合征抗原B陰性 |
JL-FA-188 | Streptolysin O Ab (ASO) | 鏈球菌溶血素O抗體 |
JL-FA-189 | Syphilis (RPR - Rapid Plasma Reagin) Positive Plasma | 梅毒（梅毒-快速血漿反應(yīng)）陽性血漿 |
JL-FA-190 | Syphilis (RPR - Rapid Plasma Reagin) Negative Plasma | 梅毒（梅毒-快速血漿反應(yīng)）陰性血漿 |
JL-FA-191 | Syphilis/ATA/T. pallidum IgG | 梅毒ATA/T，蒼白球IGG |
JL-FA-192 | Syphilis/ATA/T. pallidum IgM | 梅毒ATA/T，蒼白球IGM |
JL-FA-193 | Systemic Lupus Erythematosus (SLE) Positive | 全身性紅斑狼瘡陽性 |
JL-FA-194 | Systemic Lupus Erythematosus (SLE) Negative | 全身性紅斑狼瘡陰性 |
JL-FA-195 | TG/TPO Positive (Standard Titer 1,000 - 3000 IU/mL) | 甲狀腺球蛋白/甲狀腺過氧化物酶陽性 |
JL-FA-196 | TG/TPO Negative | 甲狀腺球蛋白/甲狀腺過氧化物酶陰性 |
JL-FA-197 | TTG (Tissue Transglutaminase) | 組織轉(zhuǎn)谷氨酰胺酶 |
JL-FA-198 | TTG (Tissue Transglutaminase) IgA | 組織轉(zhuǎn)谷氨酰胺酶 IGA |
JL-FA-199 | ToRCH (Toxo, Rubella, CMV, HSV) Positive | 優(yōu)生優(yōu)育（弓形蟲，風(fēng)疹，巨細胞，單胞）陽性 |
JL-FA-200 | ToRCH (Toxo, Rubella, CMV, HSV) Negative | 優(yōu)生優(yōu)育（弓形蟲，風(fēng)疹，巨細胞，單胞）陰性 |
JL-FA-201 | Toxoplasmosis (Toxo) | 弓形蟲病 |
JL-FA-202 | Toxoplasmosis (Toxo) IgG | 弓形蟲病IGG |
JL-FA-203 | Toxoplasmosis (Toxo) IgM | 弓形蟲病IGM |
JL-FA-204 | Thyroglobulin (TG) Positive Plasma | 甲狀腺球蛋白陽性血漿 |
JL-FA-205 | Thyroglobulin (TG) Negative | 甲狀腺球蛋白陰性 |
JL-FA-206 | Varicella-Zoster Virus (VZV) Negative | 水痘-帶狀皰疹病毒陰性 |
JL-FA-207 | Varicella-Zoster Virus (VZV) IgG | 水痘-帶狀皰疹病毒IGG |
JL-FA-208 | Varicella-Zoster Virus (VZV) IgM | 水痘-帶狀皰疹病毒IGM |
JL-FA-209 | West Nile Virus (WNV) | 西尼羅河腦炎病毒 |
JL-FA-210 | West Nile Virus (WNV) IgM | 西尼羅河腦炎病毒IGM |
美國
“這項發(fā)現(xiàn)是我的實驗室20年來的研究結(jié)果，” 加州大學(xué)圣地亞哥分校醫(yī)學(xué)院細胞和分子系的教授史蒂文·f·道迪博士說。“它*抗原抗體了一個傳統(tǒng)的認知，即一個稱為p16-細胞周期蛋白D通路(癌癥中zui常見的遺傳通路突變)促進所有腫瘤細胞的細胞周期進程的一個基本方面。”這項研究結(jié)果發(fā)表于《eLife》雜志上。
細胞周期蛋白D是在細胞復(fù)制的*階段期間合成的，被認為有助于促進復(fù)雜的，多階段的過程，其中包括與視網(wǎng)膜母細胞瘤(Rb)蛋白的相互作用，Rb蛋白的功能是通過抑制細胞周期進程防止細胞過度生長，直到細胞準備分裂。RB是一個抑癌基因。
幾個主要的癌癥相關(guān)的Rb突變和功能失調(diào)，以及細胞周期蛋白D一直被描述為促進癌癥的一個致癌基因，因為它被認為是通過一種叫做磷酸化的過程，使Rb的抑癌功能失活。
道迪和他的同事們精心計算細胞周期進程期間的磷酸鹽添加到Rb的數(shù)量。這多達14個，但科學(xué)家發(fā)現(xiàn)，細胞周期蛋白D只增加了一個單磷酸，且只有細胞周期進程的早期G1期的14個位點中的一個，基本上有14個不同亞型的Rb。單磷酸鹽的作用是激活RB，不使它失活，這個認知已超過了20年。
研究人員說，這項研究從根本上改變了對G1期細胞周期調(diào)控和許多癌癥相關(guān)的分子起源的理解。非常重要的是要明白一個基因通路的實際功能和中斷它的后果，尤其是細胞周期蛋白D的多種藥物抑制劑用于抗原抗體癌的臨床試驗測試這種情況下。
據(jù)認為，當(dāng)器官一旦*形成，腎細胞就不能夠繁殖了。但新的研究表明，腎臟在人類的整個生命中能夠進行再生和自我修復(fù)。
美國斯坦福大學(xué)干細胞生物學(xué)和再生醫(yī)學(xué)研究所，以及以色列賽克勒醫(yī)學(xué)院的研究人員展示了，腎臟如何不斷增長以及自我更新的驚人能力，這項發(fā)現(xiàn)抗原抗體了數(shù)十年來認為腎臟不能夠再生的*理論，它也打開了通向修復(fù)腎臟甚至增長的新方法。
“這些基本理論對腎臟疾病和腎臟再生有直接的影響，”論文的主要作者Yuval Rinkevich博士說。這項研究發(fā)表于2014年5月15日的《Cell Reports》雜志上。
Cell Reports:腎臟的再生能力貫穿人的一生
長期以來，人們一直認為，腎細胞在器官一旦*形成的時候就喪失了再生的能力。這項新的研究表明，腎臟在人類的整個生命中都能夠進行再生和自我修復(fù)。
“這項研究告訴我們，腎臟決不是一個靜態(tài)的器官，” 本文的高級作者、賽克勒醫(yī)學(xué)院的兒科系副教授本杰明·德克爾博士說。“令人難以置信，腎臟可以自己恢復(fù)活力，并繼續(xù)生成專門的腎細胞。”
本文的另一個高級作者是病理學(xué)和發(fā)育生物學(xué)的教授和斯坦福研究所的主任歐文·韋斯曼博士。
美國
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"This finding is the result of two decades of my laboratory's research," said Dr. Steven F. Dodi, a professor of cellular and molecular medicine at the University of California San Diego School of Medicine. "It's a compley traditional understanding of antigen-antibody, a fundamental aspect of what is known as the p16-cyclin D pathway, the most common genetic pathway mutation in cancer, that promotes the cell cycle progression of all tumor cells." The study Results published in the "eLife" magazine.
Cyclin D, which is synthesized during the first phase of cell replication, is thought to contribute to the promotion of a complex, multi-stage process including the interaction with retinoblastoma (Rb) proteins whose function is Prevent cell overgrowth by inhibiting cell cycle progression until the cell is ready for division. RB is a tumor suppressor gene.
Several major cancer-associated Rb mutations and dysfunctions, as well as cyclin D, have long been described as an oncogene that promotes cancer as it is thought to cause the tumor suppressor function of Rb through a process called phosphorylation live.
Dodi and his colleagues carefully calculated the amount of phosphate added to the Rb during the cell cycle progression. This is up to 14, but scientists have found that cyclin D only adds one monophosphate and that only one of 14 sites in the early G1 phase of the cell cycle process has essentially 14 different subtypes of Rb. The role of monophosphates is to activate RB without inactivating it, a fact that has been recognized for more than 20 years.
The researchers say the study fundamentally changed the understanding of the molecular origins of G1-phase cell cycle regulation and many cancers. It is very important to understand the actual function of a gene pathway and to disrupt its consequences, especially in the case of a clinical trial of multiple drug inhibitors of cyclin D for antigen-antibody cancer.
It is believed that when the organ is fully formed, the kidney cells can not reproduce. But new research shows that the kidneys are able to regenerate and repair themselves throughout human life.
Researchers at the Stem Cell Biology and Regenerative Medicine Institute at Stanford University in the United States and at the Scythian Institute of Medicine in Israel demonstrated how the kidneys are constantly growing and the amazing ability to self-renew, the antigenic antibody that for decades has not been able to regenerate the kidneys The accepted theory, it also opened up new ways to repair the kidneys and even growth.
"These basic theories have a direct impact on kidney disease and kidney regeneration," said lead author Yuval Rinkevich, PhD. The study was published in Cell Reports on May 15, 2014.
Cell Reports: The ability of the kidneys to regenerate throughout one's entire life
It has long been believed that kidney cells lose their ability to regenerate once the organ is fully formed. This new study shows that the kidneys are able to regenerate and repair themselves throughout human life.
"This study ls us that the kidney is by no means a static organ," said Benjamin Dinkel, a senior author of the article and associate professor of pediatrics at Seckler School of Medicine. "It's incredible that the kidneys can regain their own vitality and continue to produce specialized kidney cells."
Another top author of this article is a professor of pathology and developmental biology and Dr. Irving Weissman, director of the Stanford Institute.
