The Birt-Hogg-Dube and tuberous sclerosis complex homologs have opposing roles in amino acid homeostasis in Schizosaccharomyces pombe. - Wikidata - wikimedia - TriplyDB

The Birt-Hogg-Dube and tuberous sclerosis complex homologs have opposing roles in amino acid homeostasis in Schizosaccharomyces pombe.

The Birt-Hogg-Dube and tuberous sclerosis complex homologs have opposing roles in amino acid homeostasis in Schizosaccharomyces pombe.

http://www.wikidata.org/entity/Q55044062

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Folliculin interacts with p0071 (plakophilin-4) and deficiency is associated with disordered RhoA signalling, epithelial polarization and cytokinesis Crystal structure of folliculin reveals a hidDENN function in genetically inherited renal cancer Serine 62 is a phosphorylation site in folliculin, the Birt-Hogg-Dubé gene product Interaction of folliculin (Birt-Hogg-Dubé gene product) with a novel Fnip1-like (FnipL/Fnip2) protein Tumor suppressor FLCN inhibits tumorigenesis of a FLCN-null renal cancer cell line and regulates expression of key molecules in TGF-beta signaling BHD mutations, clinical and molecular genetic investigations of Birt-Hogg-Dubé syndrome: a new series of 50 families and a review of published reports Kidney-targeted Birt-Hogg-Dube gene inactivation in a mouse model: Erk1/2 and Akt-mTOR activation, cell hyperproliferation, and polycystic kidneys Deficiency of FLCN in mouse kidney led to development of polycystic kidneys and renal neoplasia The role of the Birt-Hogg-Dubé protein in mTOR activation and renal tumorigenesis Loss of the Birt-Hogg-Dubé tumor suppressor results in apoptotic resistance due to aberrant TGFβ-mediated transcription Folliculin controls lung alveolar enlargement and epithelial cell survival through E-cadherin, LKB1, and AMPK.Folliculin mutations are not associated with severe COPD.Topical rapamycin as a treatment for fibrofolliculomas in Birt-Hogg-Dubé syndrome: a double-blind placebo-controlled randomized split-face trial.Negative regulation of EGFR signalling by the human folliculin tumour suppressor protein Folliculin, the product of the Birt-Hogg-Dube tumor suppressor gene, interacts with the adherens junction protein p0071 to regulate cell-cell adhesion.Folliculin regulates cell-cell adhesion, AMPK, and mTORC1 in a cell-type-specific manner in lung-derived cells.Human folliculin delays cell cycle progression through late S and G2/M-phases: effect of phosphorylation and tumor associated mutations Pulmonary manifestations of Birt-Hogg-Dubé syndrome.The folliculin mutation database: an online database of mutations associated with Birt-Hogg-Dubé syndrome FLCN Maintains the Leucine Level in Lysosome to Stimulate mTORC1.Clinical Features, Genetics and Potential Therapeutic Approaches for Birt-Hogg-Dubé Syndrome.Lst4, the yeast Fnip1/2 orthologue, is a DENN-family protein.The Birt-Hogg-Dubé tumor suppressor Folliculin negatively regulates ribosomal RNA synthesis Flcn-deficient renal cells are tumorigenic and sensitive to mTOR suppression.Multiple amino acid sensing inputs to mTORC1.Birt-Hogg-Dubé syndrome: from gene discovery to molecularly targeted therapies.Loss of Folliculin Disrupts Hematopoietic Stem Cell Quiescence and Homeostasis Resulting in Bone Marrow Failure.Recruitment of folliculin to lysosomes supports the amino acid-dependent activation of Rag GTPases Absence of the Birt-Hogg-Dubé gene product is associated with increased hypoxia-inducible factor transcriptional activity and a loss of metabolic flexibility The folliculin tumor suppressor is a GAP for the RagC/D GTPases that signal amino acid levels to mTORC1.Molecular genetics and clinical features of Birt-Hogg-Dubé syndrome.Birt-Hogg-Dubé syndrome and the skin.Rag GTPase in amino acid signaling.Birt-Hogg-Dubé Syndrome: A Review of Dermatological Manifestations and Other Symptoms.FLCN: The causative gene for Birt-Hogg-Dubé syndrome.H255Y and K508R missense mutations in tumour suppressor folliculin (FLCN) promote kidney cell proliferation.Constitutional FLCN mutations in patients with suspected Birt-Hogg-Dubé syndrome ascertained for non-cutaneous manifestations

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P2860

The Birt-Hogg-Dube and tuberous sclerosis complex homologs have opposing roles in amino acid homeostasis in Schizosaccharomyces pombe.

http://www.wikidata.org/entity/Q55044062

description

2007 nî lūn-bûn

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2007年の論文

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2007年学术文章

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2007年学术文章

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2007年学术文章

@zh-hans

2007年学术文章

@zh-my

2007年学术文章

@zh-sg

2007年學術文章

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2007年學術文章

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2007年學術文章

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name

The Birt-Hogg-Dube and tuberou ...... in Schizosaccharomyces pombe.

@en

The Birt-Hogg-Dube and tuberou ...... in Schizosaccharomyces pombe.

@nl

type

label

The Birt-Hogg-Dube and tuberou ...... in Schizosaccharomyces pombe.

@en

The Birt-Hogg-Dube and tuberou ...... in Schizosaccharomyces pombe.

@nl

prefLabel

The Birt-Hogg-Dube and tuberou ...... in Schizosaccharomyces pombe.

@en

The Birt-Hogg-Dube and tuberou ...... in Schizosaccharomyces pombe.

@nl

P1433

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Journal of Biological Chemistry

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The Birt-Hogg-Dube and tuberou ...... in Schizosaccharomyces pombe.

@en

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Damir Khabibullin

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

Elizabeth Petri Henske

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

Emmanuelle Nicolas

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

Marjon van Slegtenhorst

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

Tiffiney R Hartman

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

Warren D Kruger

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P2860

Folliculin encoded by the BHD gene interacts with a binding protein, FNIP1, and AMPK, and is involved in AMPK and mTOR signaling

Rheb GTPase is a direct target of TSC2 GAP activity and regulates mTOR signaling

Insulin activation of Rheb, a mediator of mTOR/S6K/4E-BP signaling, is inhibited by TSC1 and 2

Rheb binds tuberous sclerosis complex 2 (TSC2) and promotes S6 kinase activation in a rapamycin- and farnesylation-dependent manner

Rheb is a direct target of the tuberous sclerosis tumour suppressor proteins

Mutations in a novel gene lead to kidney tumors, lung wall defects, and benign tumors of the hair follicle in patients with the Birt-Hogg-Dubé syndrome

Tuberous sclerosis complex gene products, Tuberin and Hamartin, control mTOR signaling by acting as a GTPase-activating protein complex toward Rheb

Growing roles for the mTOR pathway

mTOR and cancer: insights into a complex relationship

A 4-bp deletion in the Birt-Hogg-Dubé gene (FLCN) causes dominantly inherited spontaneous pneumothorax.

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24583-24590

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scholarly article

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10.1074/JBC.M700857200

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P433

34

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

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282

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2007-06-07T00:00:00Z

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17556368

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P921

methionine import across plasma membrane

L-methionine import across plasma membrane

regulation of L-methionine import across plasma membrane

positive regulation of L-methionine import across plasma membrane

negative regulation of L-methionine import across plasma membrane