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Plays a role in bone mineralization (By similarity).. Additionally we are shipping IFITM5 Proteins (3) and many more products for this protein.
Showing 10 out of 35 products:
Human Polyclonal IFITM5 Primary Antibody for EIA, WB - ABIN952824
Moffatt, Gaumond, Salois, Sellin, Bessette, Godin, de Oliveira, Atkins, Nanci, Thomas: Bril: a novel bone-specific modulator of mineralization. in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2008
Show all 2 references for ABIN952824
Human Polyclonal IFITM5 Primary Antibody for WB - ABIN655010
Baird, Ryan, Hayes, Hampson, Heyworth, Clark, Wootton, Ansell, Menzel, Hole, Graham: Differentiating embryonal stem cells are a rich source of haemopoietic gene products and suggest erythroid preconditioning of primitive haemopoietic stem cells. in The Journal of biological chemistry 2001
Two mutations in IFITM5 causing distinct forms of osteogenesis imperfect.
The point mutation, c.-14C>T in the 5'-untranslated region of IFITM5, is responsible for osteogenesis imperfecta (show COL1A2 Antibodies) type V in Chinese patients.
The IFITM5 5' UTR (show UTS2R Antibodies) was sequenced in 9 heterozygous subjects with osteogenesis imperfecta (show COL1A2 Antibodies) type V. Both wild-type and mutant IFITM5 mRNA transcripts were present in bone. Identical mutations have variable phenotypic expression, even within the same family.
The bone mineral density varied greatly, even within families. Our study thus highlights the phenotypic variability of OI type V caused by the IFITM5 mutation.
Recurrent mutation in the 5'-UTR (show UTS2R Antibodies) of IFITM5 causes osteogenesis imperfecta (show COL1A2 Antibodies) type V.
IFITM5 mutation is associated with Osteogenesis imperfecta (show COL1A2 Antibodies) type V.
study demonstrates the presence of a recurrent IFITM5 mutation in a population of patients with osteogenesis imperfecta (show COL1A2 Antibodies) type V; even though the disease-causing mutation is identical among patients, the interindividual phenotypic variability is considerable
A single recurrent mutation in the 5'-UTR (show UTS2R Antibodies) of IFITM5 causes osteogenesis imperfecta (show COL1A2 Antibodies) type V.
A mutation in the 5'-UTR (show UTS2R Antibodies) of IFITM5 creates an in-frame start codon and causes autosomal-dominant osteogenesis imperfecta (show COL1A2 Antibodies) type V with hyperplastic callus.
results suggest that expression of mutant IFITM5 causes abnormal skeletal development, low bone mass, and abnormal osteoblast differentiation
The purpose of the current study was to re-assess the topology, localization, and biochemical properties of BRIL and compare it to the osteogenesis imperfecta (show COL1A2 Antibodies) type V mutant in MC3T3 osteoblasts.
These results indicate that the S-palmitoylation on IFITM5 promotes the interaction with FKBP11 (show FKBP11 Antibodies).
Key roles for the Sp members and GLI2 (show GLI2 Antibodies) that possibly cooperate to activate Bril when the promoter becomes demethylated.
Natural antisense transcripts enhance bone formation by increasing sense IFITM5 transcription.
Ifitm5 deficiency might have a greater effect on prenatal bone development.
these results suggest that IFITM5 is involved not only in bone formation, but also in immune system activity.
Bril is a novel osteoblast protein and showed a role in mineralization, possibly identifying a new regulatory pathway in bone formation.
Plays a role in bone mineralization (By similarity).
interferon-induced transmembrane protein 5
, interferon induced transmembrane protein 5
, bone-restricted ifitm-like protein
, bone-restricted interferon-induced transmembrane protein-like protein
, dispanin subfamily A member 1
, bone-restricted interferon induced transmembrane protein-like protein
, fragilis family member 4
, haemopoiesis related membrane protein 1