Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis. - Wikidata - awgldk - TriplyDB

Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis.

Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis.

http://www.wikidata.org/entity/Q43729274

about

pRb inactivation in mammary cells reveals common mechanisms for tumor initiation and progression in divergent epithelia Inhibitor of cyclin-dependent kinase (CDK) interacting with cyclin A1 (INCA1) regulates proliferation and is repressed by oncogenic signaling Bmi-1 promotes neural stem cell self-renewal and neural development but not mouse growth and survival by repressing the p16Ink4a and p19Arf senescence pathways.Control of the replicative life span of human fibroblasts by p16 and the polycomb protein Bmi-1 p19ARF determines the balance between normal cell proliferation rate and apoptosis during mammary gland development Variants in the CDKN2B and RTEL1 regions are associated with high-grade glioma susceptibility Long non-coding RNA ANRIL is required for the PRC2 recruitment to and silencing of p15(INK4B) tumor suppressor gene Expression of p16(INK4a) in peripheral blood T-cells is a biomarker of human aging Hypersensitivity to contact inhibition provides a clue to cancer resistance of naked mole-rat Bmi-1 dependence distinguishes neural stem cell self-renewal from progenitor proliferation Histone demethylase JMJD3 contributes to epigenetic control of INK4a/ARF by oncogenic RAS Hmga2 promotes neural stem cell self-renewal in young but not old mice by reducing p16Ink4a and p19Arf Expression Cyclin D-Cdk4 is regulated by GATA-1 and required for megakaryocyte growth and polyploidization Epstein-Barr virus LMP1 blocks p16INK4a-RB pathway by promoting nuclear export of E2F4/5 Immortalization of mouse myogenic cells can occur without loss of p16INK4a, p19ARF, or p53 and is accelerated by inactivation of Bax Genetic alterations in pancreatic carcinoma Cellular senescence in aging and age-related disease: from mechanisms to therapy Current State of Animal (Mouse) Modeling in Melanoma Research Cross-species models of human melanoma Murine models and cell lines for the investigation of pheochromocytoma: applications for future therapies?Genetic regulation of thymocyte progenitor aging Mouse models of pancreatic cancer Disruptive chemicals, senescence and immortality Loss of CDKN2A expression is a frequent event in primary invasive melanoma and correlates with sensitivity to the CDK4/6 inhibitor PD0332991 in melanoma cell lines.Role of lncRNAs in Cellular Aging Biology of MET: a double life between normal tissue repair and tumor progression JDP2 (Jun Dimerization Protein 2)-deficient mouse embryonic fibroblasts are resistant to replicative senescence Immortalization eliminates a roadblock during cellular reprogramming into iPS cells A novel zinc finger protein Zfp277 mediates transcriptional repression of the Ink4a/arf locus through polycomb repressive complex 1 Inhibitor of differentiation 1 promotes endothelial survival in a bleomycin model of lung injury in mice Ink4a/Arf expression is a biomarker of aging SnoN functions as a tumour suppressor by inducing premature senescence ARF functions as a melanoma tumor suppressor by inducing p53-independent senescence Losses of both products of the Cdkn2a/Arf locus contribute to asbestos-induced mesothelioma development and cooperate to accelerate tumorigenesis A melanoma molecular disease model Molecular cloning and characterization of the human p19INK4dgene promoter Increasing p16INK4a expression decreases forebrain progenitors and neurogenesis during ageing Oxygen sensitivity severely limits the replicative lifespan of murine fibroblasts The yin-yang of DNA damage response: roles in tumorigenesis and cellular senescence.deltaNp73 facilitates cell immortalization and cooperates with oncogenic Ras in cellular transformation in vivo

P2860

Q21090243-883E79CC-CB4B-448D-BDA8-3E6304DD40EE Q24301328-8552948F-87EC-4C30-9260-0253EF320ACD Q24529593-E0E49A86-05CB-4478-AA9B-630F073D2402 Q24540711-AB20B5B9-2E66-4D50-9E33-8F5113D49B12 Q24564901-DDD1E85A-D8B2-4118-8A59-A7C6576D6F7C Q24630647-144022B0-71E5-4766-9E57-6347A54B7B40 Q24632383-4B31103A-3EE0-432F-AB9C-6526256A85AD Q24646862-A365A360-9624-41F4-9F8F-BC115F0FF698 Q24652899-8F79000F-716F-4764-A35A-1F4198E87C00 Q24652976-8B0FB01A-901C-4161-A167-6365304AB3FA Q24657459-C80F1261-B88D-4146-A763-FECB195F0F33 Q24658265-9077664D-CDE6-4EBD-9A0E-9E9145020C29 Q24674862-2F860944-F612-4056-B453-2D56DF4E0F1A Q24675583-A8B8ED8D-9CF1-4E0F-A4BC-474826CE5672 Q24791108-9E36DA39-B759-425E-ACA1-169060FB40D3 Q24801465-CF9DF173-AFF5-4EE2-B9A9-AD5C6B207D18 Q26773500-2757598A-A7CE-4095-B26A-2A56E4DC1904 Q26781652-EBE18212-F6EF-4FE8-B482-6EBADBE41469 Q26782090-2BB2C2C6-B8C5-4D78-B785-F3D6F0ACAB3A Q26828446-EAF963AB-FCD0-42E8-A3F2-16E4019334A5 Q26853420-0DC50383-7075-4FE4-A08C-30A477E7A40B Q26860574-8FCCAEBC-9F6A-405A-9498-E85C6BE1F28F Q27026235-0300228E-A055-4C93-A8FC-D6CBAC61458C Q27852814-A9EA1912-818B-462E-90FB-9B7A1EC4DF02 Q28078986-8D10E6B4-F673-4F3C-8A10-4AA5B6C95393 Q28085247-0414D257-6F7B-4BA6-B407-DBF0DC1D69EB Q28235883-C28E9428-27A7-428C-B3B9-4B60C2ED76D3 Q28254388-090DB007-FCE4-4D9E-8CA3-AAAB7213BC43 Q28506253-E6A921B8-A072-4210-94AA-390E28E10B4B Q28506363-B46B0FDB-BC3F-49B3-8CB5-34A482258A14 Q28570483-A9A47E32-17B1-42E0-9128-2F492ED3A37C Q28585092-6F86536F-BB50-4CC9-99DB-38917988284A Q28591778-B21117C0-0496-4FBA-A84E-B06E0E350E38 Q28740925-74A5B2AC-12D7-4220-B4A8-F0C1206E9324 Q28741507-F2FD4CB6-B8A7-4D7A-B44D-D3CFAB81183F Q29300177-2F9C7DF2-3148-48FB-AC56-A1974EB186EF Q29615155-EE009944-6FC9-4906-8397-F7EB1A1DCB86 Q29618748-19AD0181-02A3-4BFC-8505-31ED5CBAC417 Q30426400-62CDC521-7539-4FD5-A822-52526FBB98FA Q30452755-F5465A6C-FF6B-4B5C-9A99-9CFFF215FBAB

P2860

Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis.

http://www.wikidata.org/entity/Q43729274

description

2001 nî lūn-bûn

@nan

2001年の論文

@ja

2001年学术文章

@wuu

2001年学术文章

@zh-cn

2001年学术文章

@zh-hans

2001年学术文章

@zh-my

2001年学术文章

@zh-sg

2001年學術文章

@yue

2001年學術文章

@zh

2001年學術文章

@zh-hant

name

Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis.

@en

Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis.

@nl

type

label

Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis.

@en

Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis.

@nl

prefLabel

Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis.

@en

Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis.

@nl

P1433

Q43729274-F03A4106-BA96-4EE8-9392-BE22A4EF2F56

P1476

Q43729274-2002F750-F8FC-4880-9302-BD68915CC2B1

P2093

Q43729274-19AF2BDF-444A-4F25-AE8C-B54D22508A4E

Q43729274-5CD9FD2D-FC00-4ABB-87AE-0A8394D6B4F9

Q43729274-661E3283-6726-47BD-A751-7392BC7BDEF5

Q43729274-6FCC05D6-AA29-4FCD-86F9-3B03BDED2CD3

Q43729274-71585C51-B56E-4884-A394-4536C1260BC8

Q43729274-98932BE6-95EF-42E9-8DB6-C356998C29F2

Q43729274-E8FA5F0F-7784-4DA3-87C1-796257DCF292

Q43729274-FE94C284-2160-49E1-97DD-E3C003810A16

P2860

Q43729274-00BA6504-120F-4E6B-A6BC-63199415E850

Q43729274-0BF18F64-CAC5-498A-96C5-E9AC1BF3B072

Q43729274-11DF101E-2129-4088-A454-F864E229D7DE

Q43729274-1C615E5C-EE9D-4A94-87FA-F38151394472

Q43729274-27A0DFB6-CEFB-4698-92C1-AE4B0F7D8035

Q43729274-36190FDB-BFDA-4298-A48D-642E3B985007

Q43729274-3C09BC53-1E05-4682-9CB3-92E36CE05DF7

Q43729274-45432590-C8ED-4522-83ED-65BE0108CBAB

Q43729274-510F3EB0-D585-47D9-8EA8-42B52D6212F5

Q43729274-550E76D0-8945-401E-9721-564F8D756354

P2888

Q43729274-2B5553B2-7D9A-4E4A-8252-C51F5F6369FF

P304

Q43729274-DC2DD3C5-EF21-4898-8004-C77D09F58A43

P31

Q43729274-0539E477-C28D-43B1-932C-4ECE75123251

P356

Q43729274-FF8767B6-9FBA-46C1-9BF1-E5FC4D5C657F

P407

Q43729274-CEE3885D-AA70-40AD-971E-AE69C823E8B6

P433

Q43729274-8AFC3983-8C43-44DC-908C-47EDEC53FF10

P478

Q43729274-929CA32E-3898-4AC5-85A3-3C00A7369ED3

P50

Q43729274-98EC14B0-FEF7-4D22-A30B-FD18B7A539DA

P577

Q43729274-BA7014FA-F21D-4560-ABE2-E74ED846B777

P6179

Q43729274-FA91B8C8-9C05-4B24-A937-2830513BF3F9

P698

Q43729274-7ACA3040-BC5D-4132-A722-2A9B0C375BF0

P356

P1433

P1476

Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis.

@en

P2093

Aguirre AJ

http://www.w3.org/2001/XMLSchema#string

Bardeesy N

http://www.w3.org/2001/XMLSchema#string

Carrasco D

http://www.w3.org/2001/XMLSchema#string

Castrillon DH

http://www.w3.org/2001/XMLSchema#string

DePinho RA

http://www.w3.org/2001/XMLSchema#string

Horner JW

http://www.w3.org/2001/XMLSchema#string

Lee KH

http://www.w3.org/2001/XMLSchema#string

Wu EA

http://www.w3.org/2001/XMLSchema#string

P2860

Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

A biomarker that identifies senescent human cells in culture and in aging skin in vivo

Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands

Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest

Efficient in vivo manipulation of mouse genomic sequences at the zygote stage

D-type cyclin-dependent kinase activity in mammalian cells

Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF

Hypermethylation of the p16 (Ink4a) promoter in B6C3F1 mouse primary lung adenocarcinomas and mouse lung cell lines.

The INK4A/ARF locus and its two gene products.

Efficiency alleles of the Pctr1 modifier locus for plasmacytoma susceptibility

P2888

P304

86-91

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1038/35092592

http://www.w3.org/2001/XMLSchema#string

P407

P433

6851

http://www.w3.org/2001/XMLSchema#string

P478

413

http://www.w3.org/2001/XMLSchema#string

P50

Norman Sharpless

P577

2001-09-01T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P6179

1009073714

http://www.w3.org/2001/XMLSchema#string

P698

11544531

http://www.w3.org/2001/XMLSchema#string