A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
about
Hallmarks of progeroid syndromes: lessons from mice and reprogrammed cellsConnecting the Dots: From DNA Damage and Repair to AgingModeling the study of DNA damage responses in miceAdaptive stress response in segmental progeria resembles long-lived dwarfism and calorie restriction in miceDifferentiation driven changes in the dynamic organization of Basal transcription initiationRescue of progeria in trichothiodystrophy by homozygous lethal Xpd allelesIdentification of the XPG region that causes the onset of Cockayne syndrome by using Xpg mutant mice generated by the cDNA-mediated knock-in methodMutations in TFIIH causing trichothiodystrophy are responsible for defects in ribosomal RNA production and processingHypermutation of immunoglobulin genes in memory B cells of DNA repair-deficient miceHomeostatic imbalance between apoptosis and cell renewal in the liver of premature aging Xpd micePostnatal growth failure, short life span, and early onset of cellular senescence and subsequent immortalization in mice lacking the xeroderma pigmentosum group G geneAge-related skeletal dynamics and decrease in bone strength in DNA repair deficient male trichothiodystrophy miceEarly postnatal ataxia and abnormal cerebellar development in mice lacking Xeroderma pigmentosum Group A and Cockayne syndrome Group B DNA repair genesPersistence of repair proteins at unrepaired DNA damage distinguishes diseases with ERCC2 (XPD) mutations: cancer-prone xeroderma pigmentosum vs. non-cancer-prone trichothiodystrophy.p8/TTDA overexpression enhances UV-irradiation resistance and suppresses TFIIH mutations in a Drosophila trichothiodystrophy model.An Xpb mouse model for combined xeroderma pigmentosum and cockayne syndrome reveals progeroid features upon further attenuation of DNA repair.The 8,5'-cyclopurine-2'-deoxynucleosides: candidate neurodegenerative DNA lesions in xeroderma pigmentosum, and unique probes of transcription and nucleotide excision repair.Phosphorylation of steroidogenic factor 1 is mediated by cyclin-dependent kinase 7Dysregulation of the peroxisome proliferator-activated receptor target genes by XPD mutationsPremature aging and cancer in nucleotide excision repair-disorders.Age-related neuronal degeneration: complementary roles of nucleotide excision repair and transcription-coupled repair in preventing neuropathologyDeficiency in nucleotide excision repair family gene activity, especially ERCC3, is associated with non-pigmented hair fiber growth.Dynamic partnership between TFIIH, PGC-1α and SIRT1 is impaired in trichothiodystrophy.Mutant laboratory mice with abnormalities in hair follicle morphogenesis, cycling, and/or structure: annotated tables.Blinded by the UV light: how the focus on transcription-coupled NER has distracted from understanding the mechanisms of Cockayne syndrome neurologic diseaseAnalysis of osteoarthritis in a mouse model of the progeroid human DNA repair syndrome trichothiodystrophy.Ocular manifestations of trichothiodystrophyDNA-damage repair; the good, the bad, and the ugly.DDB2 gene disruption leads to skin tumors and resistance to apoptosis after exposure to ultraviolet light but not a chemical carcinogen.Do all of the neurologic diseases in patients with DNA repair gene mutations result from the accumulation of DNA damage?GTF2E2 Mutations Destabilize the General Transcription Factor Complex TFIIE in Individuals with DNA Repair-Proficient TrichothiodystrophyBone fragility and decline in stem cells in prematurely aging DNA repair deficient trichothiodystrophy miceGlobal regulation of promoter melting in naive lymphocytes.Hot topics in DNA repair: the molecular basis for different disease states caused by mutations in TFIIH and XPG.Abnormal XPD-induced nuclear receptor transactivation in DNA repair disorders: trichothiodystrophy and xeroderma pigmentosum.DNA repair is crucial for maintaining hematopoietic stem cell functionNucleotide excision repair deficient mouse models and neurological disease.DNA double-strand breaks: a potential causative factor for mammalian aging?Disruption of Supv3L1 damages the skin and causes sarcopenia, loss of fat, and death.Tissue-specific accelerated aging in nucleotide excision repair deficiency
P2860
Q26740026-E97FB6BF-0247-472F-BA90-97CB0B0D8989Q26750854-9B06F60C-2CC2-4721-81DA-67F47FBD7EE7Q26826949-C970E8B0-3FD4-4F25-953B-A8739C6EAC38Q27315126-060A9EC5-2DC4-47FA-B848-C1971BE31AFAQ27325737-ADCDE05B-D679-4EA3-93AB-6887F4D4630AQ28469053-512AD795-8F40-4428-BC8A-D66A6AA31876Q28506081-5C88B039-E127-4DBB-A945-F860E6C4B896Q28507301-9E030ECF-D5A8-4BCA-AF10-E15F474F0859Q28507519-CB692628-3ACE-4CF2-86F1-6308BBAB3E4AQ28508537-F0ED8712-D4C8-41BF-9E56-CAB4CAD975D1Q28592787-C9CEBA3F-27B8-450A-9243-44DE1F00A12CQ28730665-CBC89E05-8250-4B4B-AF0D-271EE5BDA4F9Q30759755-48CA4DD1-7411-4309-B5A2-9C583EC3637EQ33333583-5ABFAA25-4A2C-4E89-B3C3-78FC19F2D58DQ33384431-A82A9F96-BD26-4E3C-AAA9-A3106BFC4AC5Q33396433-203F2A64-FAAE-4E93-93F1-5E762A587543Q33554002-2C909DA4-6E3A-4115-94B4-AAD430F37035Q33643318-E60BB5D8-6408-4A01-AA47-AA44C7DCA5C8Q33884120-39831A41-1D93-42B0-82B4-E8EFF851A3BBQ34025252-E11199DF-812E-44EA-9524-C938CB631395Q34102796-5D8D418F-1B15-4515-B4AC-B3043DEC6A17Q34277167-1D74899C-424A-4350-BF64-EA988BA56555Q34394923-710AB7F1-ED93-450E-8FB1-FE81E11FA1ACQ34459252-0806133C-6FD5-4A34-BE03-C2A6A821C87EQ34554610-AD10E141-8941-4BD3-8C1F-298981B0C171Q35201115-12BA68FE-3F28-4CCC-8E21-131EF503C83AQ35592622-7F2561C2-DE9A-4515-834A-73E9ED48F640Q36487307-A614EF8F-60FF-448A-99FD-8E04B048AC97Q36604609-96A1CDB8-99BE-4130-8EBE-7C764D65C6FCQ36690915-1DB18EF0-8C55-40A1-ADBF-556E9D677ACBQ36802296-C9897AEC-7595-4A4D-AD13-4E73E9BE6823Q36927452-0C31F84D-C0A4-461D-9FFA-FEF981D7CF13Q36935665-02673840-8A3D-4508-8CD0-4B69BEE2F7DCQ37031123-753A09DC-8721-4E96-83DC-63D6C19BA248Q37043787-061B9968-D681-4D0E-9DA2-4545785F3973Q37076623-53E2674C-863D-4EA1-AD99-94BC6F42DE4FQ37083895-C02D445D-3E58-4EA1-A899-0443A9C17E36Q37112251-EB7010AE-58A5-4AA8-97D7-28B803D043DEQ37154170-F19E9BBF-B9E9-4B79-BA9D-590F8BDE565BQ37185712-72CCFE9D-8617-47D9-A185-D0DB90F1291E
P2860
A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
description
1998 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
1998 թվականի հունիսին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 1998
@ast
scientific journal article
@en
vedecký článok (publikovaný 1998/06/01)
@sk
vědecký článek publikovaný v roce 1998
@cs
wetenschappelijk artikel (gepubliceerd op 1998/06/01)
@nl
wissenschaftlicher Artikel
@de
наукова стаття, опублікована в червні 1998
@uk
مقالة علمية (نشرت في يونيو 1998)
@ar
name
A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
@ast
A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
@en
A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
@nl
type
label
A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
@ast
A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
@en
A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
@nl
prefLabel
A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
@ast
A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
@en
A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
@nl
P2093
P3181
P1433
P1476
A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
@en
P2093
A. R. Lehmann
H. Morreau
H. van Steeg
J. H. Hoeijmakers
J. de Boer
R. J. Berg
P304
P3181
P356
10.1016/S1097-2765(00)80098-2
P577
1998-06-01T00:00:00Z