GLI family zinc finger 3
آخر تحديث 11 Apr 2023
يتوافق مع الإرشادات التحريرية
- تنزيلتنزيل
- مشاركة
- Language
- نقاش
- نسخة صوتية
- أضف إلى المصادر المفضلة على جوجل
ال GLI3 gene belongs to a family of genes that are involved in the normal shaping (patterning) of many tissues and organs during the early stages of development before birth. To carry out this role, proteins produced from genes in the GLI family attach to specific regions of DNA and help control whether particular genes are turned on or off (gene expression). GLI proteins are called transcription factors on the basis of this action.
Normal function
ال GLI3 gene belongs to a family of genes that are involved in the normal shaping (patterning) of many tissues and organs during the early stages of development before birth. To carry out this role, proteins produced from genes in the GLI family attach to specific regions of DNA and help control whether particular genes are turned on or off (gene expression). GLI proteins are called transcription factors on the basis of this action.
Proteins in the GLI family function in the same molecular pathway as a protein called Sonic Hedgehog. This pathway is essential for early development. It plays a role in cell growth, cell specialization, and the patterning of structures such as the brain and limbs. Depending on signals from Sonic Hedgehog, the GLI3 protein can either turn on (activate) or turn off (repress) other genes. Researchers are working to identify the genes targeted by the GLI3 protein during development.
Conditions referring to this gene or chromosome
Other names
ACLS
GCPS
GLI-Kruppel family member GLI3 (Greig cephalopolysyndactyly syndrome)
GLI3_HUMAN
oncogene GLI3
PAP-A
PAPA
PAPA1
PAPB
PHS
PPDIV
zinc finger protein GLI3
Related patient information and medicines
Patient information leaflet
مرض الخلايا المنجلية
SCD is therefore a group of conditions that cause red cells إلى become sickle-shaped. Sickle cell trait is not the same as SCD or sickle cell anaemia. Sickle cell trait means you carry a single sickle cell gene, but it does not normally cause illness. The rest of this leaflet will discuss SCD, which includes فقر الدم المنجلي and the other less.
Patient information leaflet
السعال ونزلات البرد عند الأطفال
This is distressing but it does not necessarily indicate that they need additional treatment from a doctor. Other treatments زنك supplements Previous research studies suggest that a mineral called الزنك appears to reduce the severity of cold symptoms in healthy children. A recent review of the research on الزنك supplements and the common cold found.
Patient information leaflet
التهاب الحفاضات
Most babies develop a nappy rash at some stage. Usually it is mild and does not bother your baby. However, it can be more severe and sore in some cases. Ideally, rub on a thin layer of barrier cream or ointment just before putting on each nappy. Do not apply too much, as this may reduce the 'breathability' of the nappy. The recommended ointments.
Patient information leaflet
تساقط الشعر الكربي
Telogen effluvium (hair loss) is a condition where more than normal amounts of hair fall out. There is a general 'thinning' of the hair. Unlike some other hair and scalp conditions, it is temporary and the hair growth usually recovers. What is telogen effluvium. Telogen effluvium is rapid hair loss that is caused by stress or a change to your.
Patient information leaflet
رائحة الفم الكريهة
For example, they may. People with halitophobia often become fixa... Gum disease is a common cause of halitosis و أ dentist will be able to advise on treatment if you have gum disease. A number of clinical trials have shown that various ingredients are good at reducing bad breath. These include chlorhexidine, cetylpyridinium chloride, chlorine.
Patient information leaflet
تصلب الجلد الجهازي
Normally, our body makes proteins called antibodies to fight infections - for example, when we catch a cold or have a sore throat. These antibodies help to kill the germs causing the infection. In autoimmune diseases the body makes similar antibodies (autoantibodies) that attack its normal cells. In systemic sclerosis, the immune system damages.
قراءة إضافية ومراجع
- GLI family zinc finger 3; MedlinePlus, National Library of Medicine.
- Biesecker LG, Johnston J. Syndromic and non-syndromic GLI3 phenotypes. Clin Genet. 2005 Sep;68(3):284; author reply 285. doi: 10.1111/j.1399-0004.2005.0485a.x. No abstract available.
- Biesecker LG, Johnston JJ. GLI3-Related Greig Cephalopolysyndactyly Syndrome. 2001 Jul 9 [updated 2025 Aug 28]. In: Adam MP, Bick S, Mirzaa GM, Wallace SE, Amemiya A, editors. GeneReviews(R) [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from http://www.ncbi.nlm.nih.gov/books/NBK1446/
- Biesecker LG. GLI3-Related Pallister-Hall Syndrome. 2000 May 25 [updated 2024 Feb 22]. In: Adam MP, Bick S, Mirzaa GM, Wallace SE, Amemiya A, editors. GeneReviews(R) [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from http://www.ncbi.nlm.nih.gov/books/NBK1465/
- Demurger F, Ichkou A, Mougou-Zerelli S, Le Merrer M, Goudefroye G, Delezoide AL, Quelin C, Manouvrier S, Baujat G, Fradin M, Pasquier L, Megarbane A, Faivre L, Baumann C, Nampoothiri S, Roume J, Isidor B, Lacombe D, Delrue MA, Mercier S, Philip N, Schaefer E, Holder M, Krause A, Laffargue F, Sinico M, Amram D, Andre G, Liquier A, Rossi M, Amiel J, Giuliano F, Boute O, Dieux-Coeslier A, Jacquemont ML, Afenjar A, Van Maldergem L, Lackmy-Port-Lis M, Vincent-Delorme C, Chauvet ML, Cormier-Daire V, Devisme L, Genevieve D, Munnich A, Viot G, Raoul O, Romana S, Gonzales M, Encha-Razavi F, Odent S, Vekemans M, Attie-Bitach T. New insights into genotype-phenotype correlation for GLI3 mutations. Eur J Hum Genet. 2015 Jan;23(1):92-102. doi: 10.1038/ejhg.2014.62. Epub 2014 Apr 16.
- Elson E, Perveen R, Donnai D, Wall S, Black GC. De novo GLI3 mutation in acrocallosal syndrome: broadening the phenotypic spectrum of GLI3 defects and overlap with murine models. J Med Genet. 2002 Nov;39(11):804-6. doi: 10.1136/jmg.39.11.804.
- Johnston JJ, Olivos-Glander I, Killoran C, Elson E, Turner JT, Peters KF, Abbott MH, Aughton DJ, Aylsworth AS, Bamshad MJ, Booth C, Curry CJ, David A, Dinulos MB, Flannery DB, Fox MA, Graham JM, Grange DK, Guttmacher AE, Hannibal MC, Henn W, Hennekam RC, Holmes LB, Hoyme HE, Leppig KA, Lin AE, Macleod P, Manchester DK, Marcelis C, Mazzanti L, McCann E, McDonald MT, Mendelsohn NJ, Moeschler JB, Moghaddam B, Neri G, Newbury-Ecob R, Pagon RA, Phillips JA, Sadler LS, Stoler JM, Tilstra D, Walsh Vockley CM, Zackai EH, Zadeh TM, Brueton L, Black GC, Biesecker LG. Molecular and clinical analyses of Greig cephalopolysyndactyly and Pallister-Hall syndromes: robust phenotype prediction from the type and position of GLI3 mutations. Am J Hum Genet. 2005 Apr;76(4):609-22. doi: 10.1086/429346. Epub 2005 Feb 28.
- Johnston JJ, Sapp JC, Turner JT, Amor D, Aftimos S, Aleck KA, Bocian M, Bodurtha JN, Cox GF, Curry CJ, Day R, Donnai D, Field M, Fujiwara I, Gabbett M, Gal M, Graham JM, Hedera P, Hennekam RC, Hersh JH, Hopkin RJ, Kayserili H, Kidd AM, Kimonis V, Lin AE, Lynch SA, Maisenbacher M, Mansour S, McGaughran J, Mehta L, Murphy H, Raygada M, Robin NH, Rope AF, Rosenbaum KN, Schaefer GB, Shealy A, Smith W, Soller M, Sommer A, Stalker HJ, Steiner B, Stephan MJ, Tilstra D, Tomkins S, Trapane P, Tsai AC, Van Allen MI, Vasudevan PC, Zabel B, Zunich J, Black GC, Biesecker LG. Molecular analysis expands the spectrum of phenotypes associated with GLI3 mutations. Hum Mutat. 2010 Oct;31(10):1142-54. doi: 10.1002/humu.21328.
- Kang S, Graham JM Jr, Olney AH, Biesecker LG. GLI3 frameshift mutations cause autosomal dominant Pallister-Hall syndrome. Nat Genet. 1997 Mar;15(3):266-8. doi: 10.1038/ng0397-266.
- Kang S, Rosenberg M, Ko VD, Biesecker LG. Gene structure and allelic expression assay of the human GLI3 gene. Hum Genet. 1997 Dec;101(2):154-7. doi: 10.1007/s004390050605.
- Radhakrishna U, Bornholdt D, Scott HS, Patel UC, Rossier C, Engel H, Bottani A, Chandal D, Blouin JL, Solanki JV, Grzeschik KH, Antonarakis SE. The phenotypic spectrum of GLI3 morphopathies includes autosomal dominant preaxial polydactyly type-IV and postaxial polydactyly type-A/B; No phenotype prediction from the position of GLI3 mutations. Am J Hum Genet. 1999 Sep;65(3):645-55. doi: 10.1086/302557.
- Speksnijder L, Cohen-Overbeek TE, Knapen MF, Lunshof SM, Hoogeboom AJ, van den Ouwenland AM, de Coo IF, Lequin MH, Bolz HJ, Bergmann C, Biesecker LG, Willems PJ, Wessels MW. A de novo GLI3 mutation in a patient with acrocallosal syndrome. Am J Med Genet A. 2013 Jun;161A(6):1394-400. doi: 10.1002/ajmg.a.35874. Epub 2013 Apr 30.
- Wild A, Kalff-Suske M, Vortkamp A, Bornholdt D, Konig R, Grzeschik KH. Point mutations in human GLI3 cause Greig syndrome. Hum Mol Genet. 1997 Oct;6(11):1979-84. doi: 10.1093/hmg/6.11.1979.
تاريخ المقال
المقال متاح أيضًا باللغة الإنجليزية, الألمانية, إسبانية, الفرنسية, إيطالي, البرتغالية, الهندية, العبرية, العربية ,، و السويدية.
11 Apr 2023 | أحدث إصدار
1 Jan 2017 | 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.