ライフサイエンスコーパス: FOP

1 FOP (FGFR1 Oncogene Partner) is a known centrosome prote

2 FOP mutations break critical interactions that stabilize

3 FOP showed high uptake and slow clearance of radioactivi

4 FOP-associated mutations in the BMP receptor ALK2 reduce

5 FOP-FGFR1, an oncogenic fusion that causes a form of leu

6 n-specific enolase (NSE) promoter develops a FOP-like phenotype.

7 by twinned, N-terminal TOF (TON1, OFD1, and FOP) and LisH motifs, motifs that otherwise facilitate l

8 As for BBS4, FOP localization to satellites is cell cycle dependent,

9 derstanding and drug development hard-won by FOP researchers to pediatric neurooncology.

10 liopathy protein, CEP19, we identify CEP350, FOP, and the RABL2B GTPase as proteins organizing the fi

11 to the ciliary base by the centriolar CEP350/FOP complex and then specifically captures GTP-bound RAB

12 s significantly more active than the classic FOP mutation ACVR1(R206H) when overexpressed in chicken

13 that the ACVR1(Q207E) resembles the classic FOP receptor in these assays, not the engineered ACVR1(Q

14 cated in a codon adjacent to the most common FOP mutation [c.617G>A, p.R206H] of Activin A Receptor,

15 When iodide-bridged dimer FOP precatalysts are activated by reaction with excess s

16 p.Q207D-c.a. mice have served as a model for FOP HO in several in vivo studies.

17 tation has severe limitations as a model for FOP, whereas the naturally occurring mutations p.R206H a

18 rminal M2 motif of CAP350 is responsible for FOP recruitment at the centrosome.

19 by liver and the high sensitivity of hepatic FOP DV to changes of HMFAO with CPT-I inhibition and hyp

20 sion that the mutant R206H ACVR1 receptor in FOP patients is an activating mutation that induces BMP

21 esis, osteogenesis and joint fusions seen in FOP.

22 We mapped FOP to chromosome 2q23-24 by linkage analysis and identi

23 ssays revealed that both naturally occurring FOP receptors (ACVR1(R206H) and ACVR1(Q207E)) were activ

24 our understanding of the clinical aspects of FOP.

25 Although the genetic defects of FOP are not known, several lines of evidence have sugges

26 Depletion of FOP strongly inhibits primary cilium formation in human

27 to clarify the intracellular disposition of FOP in the liver and test its validity as a tracer of HM

28 tor regulation and to address the effects of FOP mutation, we determined the crystal structure of the

29 mmol/L), the externally measured kinetics of FOP showed reversible binding in tissue.

30 ly small levels of diffusible metabolites of FOP were formed in vivo and in isolated rat liver.

31 The selective uptake of FOP by liver and the high sensitivity of hepatic FOP DV

32 ased on a ferrocenyloxazoline palladacyclic (FOP) scaffold were synthesized and evaluated for the rea

33 r-added 15-[18F]fluoro-3-oxa-pentadecanoate (FOP) was synthesized and evaluated in living rats and is

34 order fibrodysplasia ossificans progressiva (FOP) and have been shown to constitutively activate the

35 ns of fibrodysplasia ossificans progressiva (FOP) in human history are unknown but the condition has

36 assic fibrodysplasia ossificans progressiva (FOP) is a congenital syndrome resulting from highly cons

37 Fibrodysplasia ossificans progressiva (FOP) is a disabling genetic disorder of progressive hete

38 Fibrodysplasia ossificans progressiva (FOP) is a rare autosomal dominant disorder of skeletal m

39 Fibrodysplasia ossificans progressiva (FOP) is a rare but devastating disorder of extraskeletal

40 Fibrodysplasia ossificans progressiva (FOP) is a rare hereditary connective tissue disease char

41 Fibrodysplasia ossificans progressiva (FOP) is a severely disabling, autosomal-dominant disorde

42 s for fibrodysplasia ossificans progressiva (FOP), a debilitating and progressive heterotopic ossific

43 with fibrodysplasia ossificans progressiva (FOP), a disease in which heterotopic ossification occurs

44 ) and fibrodysplasia ossificans progressiva (FOP), respectively.

45 drome fibrodysplasia ossificans progressiva (FOP), resulting in the transformation of soft tissue int

46 Crossover events localize the putative FOP gene within a 36-cM interval bordered proximally by

47 We find that FOP partially co-localizes with the satellite component

48 These results suggest that FOP is a centriolar satellite cargo protein and, as for

49 The FOP phenotype is linked to markers located in the 4q27-3

50 To identify the chromosomal location of the FOP gene, we conducted a genomewide linkage analysis, us

51 Male-to-male transmission of the FOP phenotype excluded X-linked inheritance.

52 Localization of the FOP-FGFR1 fusion kinase to centriolar satellites may be

53 along with TrkC-miR2 overexpression and TOP/FOP flash assays confirmed the positive effect of TrkC-m

54 ent, with few satellites labeled in G1, when FOP protein levels are lowest, and most labeled in G2.

55 diverse ALK2 mutant proteins associated with FOP and DIPG.

56 a human centrosomal protein interacting with FOP, and the C-terminal M2 motif of CAP350 is responsibl

57 (TON1) proteins, which share similarity with FOP, a human centrosomal protein, are essential for micr