mitochondrially encoded NADH dehydrogenase 6
آخر تحديث 18 أبريل 2023
يتوافق مع الإرشادات التحريرية
- تنزيلتنزيل
- مشاركة
- Language
- نقاش
- نسخة صوتية
- أضف إلى المصادر المفضلة على جوجل
ال MT-ND6 gene provides instructions for making a protein called NADH dehydrogenase 6. This protein is part of a large enzyme complex known as complex I, which is active in mitochondria. Mitochondria are structures within cells that convert the energy from food into a form that cells can use. These cellular structures produce energy through a process called oxidative phosphorylation, which uses oxygen and simple sugars to create adenosine triphosphate (ATP), the cell's main energy source.
Normal function
ال MT-ND6 gene provides instructions for making a protein called NADH dehydrogenase 6. This protein is part of a large enzyme complex known as complex I, which is active in mitochondria. Mitochondria are structures within cells that convert the energy from food into a form that cells can use. These cellular structures produce energy through a process called oxidative phosphorylation, which uses oxygen and simple sugars to create adenosine triphosphate (ATP), the cell's main energy source.
Complex I is one of several enzyme complexes necessary for oxidative phosphorylation. Within mitochondria, these complexes are embedded in a tightly folded, specialized membrane called the inner mitochondrial membrane. During oxidative phosphorylation, mitochondrial enzyme complexes carry out chemical reactions that drive the production of ATP. Specifically, they create an unequal electrical charge on either side of the inner mitochondrial membrane through a step-by-step transfer of negatively charged particles called electrons. This difference in electrical charge provides the energy for ATP production.
Complex I is responsible for the first step in the electron transport process, the transfer of electrons from a molecule called NADH to another molecule called ubiquinone. Electrons are then passed from ubiquinone through several other enzyme complexes to provide energy for the generation of ATP.
Conditions referring to this gene or chromosome
Other names
mitochondrially encoded NADH dehydrogenase 6
MTND6
NADH dehydrogenase 6
NADH dehydrogenase subunit 6
NADH-ubiquinone oxidoreductase chain 6
NADH-ubiquinone oxidoreductase, subunit ND6
ND6
NU6M_HUMAN
Related patient information and medicines
Patient information leaflet
سرطان الخصية
سرطان الخصية is a السرطان that arises from a testicle (testis). Around half of all cases occur in men aged under 35 but testicular cancer rarely occurs before puberty. It is the most common cancer in men aged 15-44 years. There are about 2,000 new cases in the UK each year. The common early symptom of testicular cancer is a painless lump that.
Patient information leaflet
التخطيط للحمل
Spinal muscular atrophy. Duchenne muscular dystrophy. Fragile X syndrome. Haemophilias A and B. Glucose-6-phosphate dehydrogenase deficiency. Other medical conditions Other conditions for which it is best to see a doctor before becoming pregnant include: Thyroid problems - an underactive thyroid gland (hypothyroidism) or an overactive thyroid.
Patient information leaflet
اليرقان
It is vital to diagnose the cause of اليرقان and therefore important to always seek medical help. Jaundice treatment and outlook (prognosis) depends on the cause. What is jaundice. Causes of Jaundice It is useful to divide the causes of jaundice into four general areas: Conditions affecting the red blood cells. Conditions affecting the liver.
Patient information leaflet
هل يمكنني تناول الجلوكوزامين وفيتامين سي معًا؟
Kidney stones (oxalate) High doses of Vitamin C (typically over 1000mg daily) can increase the amount of oxalate in your urine, significantly raising the risk of developing kidney stones if you are prone to them. G6PD deficiency If you have glucose-6-phosphate dehydrogenase (G6PD) deficiency, high doses of vitamin C can cause your red blood cells.
Patient information leaflet
هل يمكنني تناول زيت زهرة الربيع المسائية وفيتامين سي معًا؟
It is generally considered safe to take these two supplements together. Why this happens Evening primrose oil is a source من omega-6 fatty acids (specifically gamma-linolenic acid), while vitamin C is a water-soluble antioxidant. They are processed by the body through different pathways and do not interfere with each other's absorption,.
Patient information leaflet
هل يمكنني تناول مخلب الشيطان وفيتامين سي معًا؟
Kidney stones (oxalate) High doses of vitamin C can increase the amount of oxalate in your urine, significantly raising the risk of developing kidney stones, especially if you have a history of them. G6PD deficiency If you have glucose-6-phosphate dehydrogenase (G6PD) deficiency, high doses of vitamin C can cause your red blood cells to break down.
قراءة إضافية ومراجع
- mitochondrially encoded NADH dehydrogenase 6; MedlinePlus, National Library of Medicine.
- Baracca A, Solaini G, Sgarbi G, Lenaz G, Baruzzi A, Schapira AH, Martinuzzi A, Carelli V. Severe impairment of complex I-driven adenosine triphosphate synthesis in leber hereditary optic neuropathy cybrids. Arch Neurol. 2005 May;62(5):730-6. doi: 10.1001/archneur.62.5.730.
- Carelli V, Ghelli A, Bucchi L, Montagna P, De Negri A, Leuzzi V, Carducci C, Lenaz G, Lugaresi E, Degli Esposti M. Biochemical features of mtDNA 14484 (ND6/M64V) point mutation associated with Leber's hereditary optic neuropathy. Ann Neurol. 1999 Mar;45(3):320-8.
- Chinnery PF, Andrews RM, Turnbull DM, Howell NN. Leber hereditary optic neuropathy: Does heteroplasmy influence the inheritance and expression of the G11778A mitochondrial DNA mutation? Am J Med Genet. 2001 Jan 22;98(3):235-43. doi: 10.1002/1096-8628(20010122)98:33.0.co;2-o.
- Fauser S, Leo-Kottler B, Besch D, Luberichs J. Confirmation of the 14568 mutation in the mitochondrial ND6 gene as causative in Leber's hereditary optic neuropathy. Ophthalmic Genet. 2002 Sep;23(3):191-7. doi: 10.1076/opge.23.3.191.7881.
- Gropman A, Chen TJ, Perng CL, Krasnewich D, Chernoff E, Tifft C, Wong LJ. Variable clinical manifestation of homoplasmic G14459A mitochondrial DNA mutation. Am J Med Genet A. 2004 Feb 1;124A(4):377-82. doi: 10.1002/ajmg.a.20456.
- Huoponen K. Leber hereditary optic neuropathy: clinical and molecular genetic findings. Neurogenetics. 2001 Jul;3(3):119-25. doi: 10.1007/s100480100115.
- Kirby DM, Kahler SG, Freckmann ML, Reddihough D, Thorburn DR. Leigh disease caused by the mitochondrial DNA G14459A mutation in unrelated families. Ann Neurol. 2000 Jul;48(1):102-4.
- Lenaz G, Baracca A, Carelli V, D'Aurelio M, Sgarbi G, Solaini G. Bioenergetics of mitochondrial diseases associated with mtDNA mutations. Biochim Biophys Acta. 2004 Jul 23;1658(1-2):89-94. doi: 10.1016/j.bbabio.2004.03.013.
- Mitchell AL, Elson JL, Howell N, Taylor RW, Turnbull DM. Sequence variation in mitochondrial complex I genes: mutation or polymorphism? J Med Genet. 2006 Feb;43(2):175-9. doi: 10.1136/jmg.2005.032474. Epub 2005 Jun 21.
- Tarnopolsky MA, Baker SK, Myint T, Maxner CE, Robitaille J, Robinson BH. Clinical variability in maternally inherited leber hereditary optic neuropathy with the G14459A mutation. Am J Med Genet A. 2004 Feb 1;124A(4):372-6. doi: 10.1002/ajmg.a.20449.
- Valentino ML, Avoni P, Barboni P, Pallotti F, Rengo C, Torroni A, Bellan M, Baruzzi A, Carelli V. Mitochondrial DNA nucleotide changes C14482G and C14482A in the ND6 gene are pathogenic for Leber's hereditary optic neuropathy. Ann Neurol. 2002 Jun;51(6):774-8. doi: 10.1002/ana.10193.
تاريخ المقال
المقال متاح أيضًا باللغة الإنجليزية, الألمانية, إسبانية, الفرنسية, إيطالي, البرتغالية, الهندية, العبرية, العربية ,، و السويدية.
18 أبريل 2023 | أحدث إصدار
1 Aug 2006 | نُشر في الأصل
انضم إلى المحادثة
شارك أفكارك أو تجاربك مع الآخرين في مجتمعات المرضى.
اسأل، شارك، تواصل.
تصفح المناقشات، اطرح الأسئلة، وشارك التجارب عبر مئات المواضيع الصحية.
اشترك في النشرة الإخبارية للمرضى
جرعتك الأسبوعية من النصائح الصحية الواضحة والموثوقة - مكتوبة لمساعدتك على الشعور بالاطلاع والثقة والتحكم.
من خلال الاشتراك، فإنك تقبل سياسة الخصوصية. يمكنك إلغاء الاشتراك في أي وقت. نحن لا نبيع بياناتك أبدًا.