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ANKH encodes a multipass transmembrane protein that is expressed in joints and other tissues and controls pyrophosphate levels in cultured cells. Additionally we are shipping ANKH Antibodies (32) and many more products for this protein.
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Data indicate that ankylosis gene product ANK siRNA suppressed basal and hypotonically-stressed ATP levels.
This study validates the association between a functional polymorphism in the 5' UTR of ANKH and Chondrocalcinosis
Polymorphisms in ALP (show ALP Proteins), ENPP1 (show ENPP1 Proteins) and ANKH are important genetic risk factors contributing to Pseudoxanthoma elasticum
ANK was concentrated around crystal deposits and correlated with markers of chondrocyte hypertrophy. These findings support a role for ANK in CPPD crystal formation in cartilage.
expression levels of type II collagen (show COL2A1 Proteins), aggrecan (show ACAN Proteins), and ANK in endplate chondrocytes of experimental group were lower than that of control group and phosphorylation level of JNK (show MAPK8 Proteins) in the experimental group which was higher than that in the control group
Analysis of the present CMD (show ACAN Proteins) family suggested the presence of a maternal mosaicism in an ANKH mutation, and the mother who was mosaic for the ANKH mutation had no apparent clinical or radiological features of CMD (show ACAN Proteins).
The aim of this study was to investigate two mineralization-related genes TNAP and ANKH polymorphisms associated with ankylosing spondylitis (AS) in the North Chinese Han population.
Neither ANKH nor ENPP1 (show ENPP1 Proteins) mutations are the cause of chondrocalcinosis in these Slovakian families.
TNF (show TNF Proteins)-activated NF-kappaB (show NFKB1 Proteins) promotes inflammation-accelerated vascular calcification by inhibiting ankylosis protein homolog expression and consequent pyrophosphate secretion.
We report a novel mutation, not previously described, in ANKH exon 1, wherein serine replaces proline, in a case of early-onset severe calcium pyrophosphate disease associated with metabolic abnormalities, with similar findings in the proband's father
These results confirm data in white Europeans that ANKH is probably not a major determinant of susceptibility to ankylosing spondylitis.
regulates the transport of inorganic pyrophosphate, and Ank knock-out mice feature a rapidly forming and thick cementum and increased cementum regeneration
Loss of Ank alters cementoblast gene expression and cervical cementum extracellular matrix composition.
the relationship between the type of temporomandibular disorders (TMD (show TTN Proteins)) and ANKH polymorphisms
Phe377del mutation in ANK causes impaired osteoblastogenesis and osteoclastogenesis resulting in hypomineralization and a high bone mass phenotype.
ANK is a positive regulator of osteoblastic and osteoclastic differentiation events toward a mature osteoblastic and osteoclastic phenotype.
Analyses on mineralized tissues showed no decrease in mineralization between ank/ank cementum vs. WT controls. Nanoindentation on enamel, dentin or cementum of ank/ank vs. WT molars revealed no significant difference in hardness and elastic modulus.
endogenous expression of ANKH mRNA and protein in whole mouse kidney as well as mouse renal epithelial cell lines and a osteoblast cell line.
Linked regulatory effects on extracellular PP(i) and OPN expression mediate the ability of PC-1 and ANK to regulate calcification.
intra-renal and subcellular localisation of ANK is consistent with pyrophosphate export from collecting duct cells and supports a role for ANK in limiting intra-renal calcium-crystal formation
These results revealed a novel function of ANKH in the promotion of early erythroid differentiation and that ank/ank mice have lower serum levels of Epo than the normal littermates, and this is the likely cause of microcytosis in these mutant mice.
This gene encodes a multipass transmembrane protein that is expressed in joints and other tissues and controls pyrophosphate levels in cultured cells. Progressive ankylosis-mediated control of pyrophosphate levels has been suggested as a possible mechanism regulating tissue calcification and susceptibility to arthritis in higher animals. Mutations in this gene have been associated with autosomal dominant craniometaphyseal dysplasia.
ankylosis, progressive homolog (mouse)
, progressive ankylosis protein
, progressive ankylosis protein homolog-like
, progressive ankylosis protein homolog
, ankylosis, progressive homolog
, progressive ankylosis-like protein
, progressive ankylosis homolog
, progressive ankylosis protein homolog B
, fn54 protein