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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Folliculin interacting protein 1

Top mentioned proteins: folliculin, mTOR, AMPK, ACID, CAN
Papers on FNIP1
Birt-Hogg-Dubé syndrome: Clinical and molecular aspects of recently identified kidney cancer syndrome.
Yao et al., Yokohama, Japan. In Int J Urol, Dec 2015
Recent studies using murine models for FLCN, a protein encoded by the FLCN gene, and its two binding partners, folliculin-interacting protein 1 (FNIP1) and folliculin-interacting protein 2 (FNIP2), have uncovered important roles for FLCN, FNIP1 and FNIP2 in cell metabolism, which include AMP-activated protein kinase-mediated energy sensing, Ppargc1a-driven mitochondrial oxidative phosphorylation and mTORC1-dependent cell proliferation.
TDP-43 affects splicing profiles and isoform production of genes involved in the apoptotic and mitotic cellular pathways.
Buratti et al., Trieste, Italy. In Nucleic Acids Res, Nov 2015
Validation of the data, both in neuronal and non-neuronal cell lines demonstrated that TDP-43 substantially alters the levels of isoform expression in four genes potentially important for neuropathology: MADD/IG20, STAG2, FNIP1 and BRD8.
Molecular genetics and clinical features of Birt-Hogg-Dubé syndrome.
Linehan et al., Bethesda, United States. In Nat Rev Urol, Oct 2015
FLCN interacts with two novel proteins, FNIP1 and FNIP2, and with AMPK, a negative regulator of mTOR.
Folliculin-interacting proteins Fnip1 and Fnip2 play critical roles in kidney tumor suppression in cooperation with Flcn.
Schmidt et al., Kumamoto, Japan. In Proc Natl Acad Sci U S A, May 2015
Folliculin (FLCN)-interacting proteins 1 and 2 (FNIP1, FNIP2) are homologous binding partners of FLCN, a tumor suppressor for kidney cancer.
Clinical Features, Genetics and Potential Therapeutic Approaches for Birt-Hogg-Dubé Syndrome.
Linehan et al., Bethesda, United States. In Expert Opin Orphan Drugs, 2014
Novel FLCN-interacting proteins, FNIP1 and FNIP2, were identified.
The folliculin tumor suppressor is a GAP for the RagC/D GTPases that signal amino acid levels to mTORC1.
Sabatini et al., Cambridge, United States. In Mol Cell, 2013
We identify FLCN and its binding partners, FNIP1/2, as Rag-interacting proteins with GAP activity for RagC/D, but not RagA/B.
Recruitment of folliculin to lysosomes supports the amino acid-dependent activation of Rag GTPases.
Ferguson et al., New Haven, United States. In J Cell Biol, 2013
FLCN-interacting protein 1 (FNIP1) promotes both the lysosome recruitment and Rag interactions of FLCN.
Birt-Hogg-Dubé syndrome: from gene discovery to molecularly targeted therapies.
Schmidt, Frederick, United States. In Fam Cancer, 2013
The identification of novel FLCN interacting proteins FNIP1 and FNIP2/L and their interaction with 5'-AMP activated protein kinase (AMPK) has provided a link between FLCN and the AMPK-mTOR axis and suggested molecular targets for therapeutic intervention to treat BHD kidney cancer and fibrofolliculomas.
Birt-Hogg-Dube syndrome: clinicopathological features of the lung.
Nakatani et al., Yokohama, Japan. In J Clin Pathol, 2013
FLCN forms a complex with FLCN-interacting protein 1 (FNIP1) and FNIP2 (also known as FNIPL), and the complex cross-talks with signalling molecules such as 5'-AMP-activated protein kinase (AMPK) and the mammalian target of rapamycin (mTOR).
MBNL1 and RBFOX2 cooperate to establish a splicing programme involved in pluripotent stem cell differentiation.
Tazi et al., Montpellier, France. In Nat Commun, 2012
These critical splicing adjustments arise early in vertebrate evolution and remain fixed in at least 10 genes (including PLOD2, CLSTN1, ATP2A1, PALM, ITGA6, KIF13A, FMNL3, PPIP5K1, MARK2 and FNIP1), implying that vertebrates require alternative splicing to fully implement the instructions of transcriptional control networks.
The folliculin-FNIP1 pathway deleted in human Birt-Hogg-Dubé syndrome is required for murine B-cell development.
Casellas et al., Bethesda, United States. In Blood, 2012
The FLCN-FNIP complex deregulated in Birt-Hogg-Dube syndrome is absolutely required for B-cell differentiation.
Discovery of Novel DENN Proteins: Implications for the Evolution of Eukaryotic Intracellular Membrane Structures and Human Disease.
Aravind et al., Bethesda, United States. In Front Genet, 2011
Of these, SMCR8, the folliculin interacting protein-1 and 2 (FNIP1 and FNIP2), nitrogen permease regulator 2 (NPR2), and NPR3 are proposed to function in recruiting Rab GTPases during different steps of autophagy, fusion of autophagosomes with the vacuole and regulation of cellular metabolism.
The genetic basis of kidney cancer: a metabolic disease.
Schmidt et al., Bethesda, United States. In Nat Rev Urol, 2010
The FLCN-FNIP1-FNIP2 complex binds AMPK and, therefore, might interact with the cellular energy and nutrient sensing pathways AMPK-TSC1/2-mTOR and PI3K-Akt-mTOR.
Serine 62 is a phosphorylation site in folliculin, the Birt-Hogg-Dubé gene product.
Hino et al., Tokyo, Japan. In Febs Lett, 2010
By binding with FLCN-interacting proteins (FNIP1 and FNIP2/FNIPL), Ser62 phosphorylation is increased.
Interaction of folliculin (Birt-Hogg-Dubé gene product) with a novel Fnip1-like (FnipL/Fnip2) protein.
Hino et al., Tokyo, Japan. In Oncogene, 2008
The function of folliculin (Flcn), encoded by BHD, is totally unknown, although its interaction with Fnip1 has been reported.
Folliculin encoded by the BHD gene interacts with a binding protein, FNIP1, and AMPK, and is involved in AMPK and mTOR signaling.
Zbar et al., Frederick, United States. In Proc Natl Acad Sci U S A, 2006
Results suggest that FLCN, mutated in Birt-Hogg-Dube syndrome, and its interacting partner FNIP1 may be involved in energy and/or nutrient sensing through the AMPK and mTOR signaling pathways.
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