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SAMD9 encodes a sterile alpha motif domain-containing protein. Additionally we are shipping and many more products for this protein.
Showing 10 out of 39 products:
Human Polyclonal SAMD9 Primary Antibody for ICC, IF - ABIN4351962
Jiang, Opanubi, Coombs: Non-Biased Enrichment Does Not Improve Quantitative Proteomic Delineation of Reovirus T3D-Infected HeLa Cell Protein Alterations. in Frontiers in microbiology 2012
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Human Polyclonal SAMD9 Primary Antibody for IHC (p), WB - ABIN651896
Topaz, Indelman, Chefetz, Geiger, Metzker, Altschuler, Choder, Bercovich, Uitto, Bergman, Richard, Sprecher: A deleterious mutation in SAMD9 causes normophosphatemic familial tumoral calcinosis. in American journal of human genetics 2006
Progressive loss of mutated SAMD9 through the development of monosomy 7 (-7), deletions of 7q (7q-), and secondary somatic loss-of-function (nonsense and frameshift) mutations in SAMD9 rescued the growth-restricting effects of mutant SAMD9 proteins in bone marrow and was associated with increased length of survival.
SAMD9 mutation is associated with MIRAGE syndrome.
Replication of the K1L(-)C7L(-) mutant vaccinia virus virus was enabled by multiple siRNAs to SAMD9 or WDR6 (show WDR6 Antibodies).
SAMD9 is down-regulated in non-small cell lung cancer. Knockdown of SAMD9 expression increased the invasion, migration and proliferation in H1299 cells in vitro and overexpression of SAMD9 suppressed proliferation and invasion in A549 cells.
When SAMD9 is stimulated due to failure of the viral antagonism during infection, the resulting antiviral granules exhibit properties different from those of the canonical stress granules.
Over-expression of SAMD9 is correlated with the metastasis of esophageal squamous cell carcinoma
M062 also binds and antagonizes cellular SAMD9 in human cells, suggesting that SAMD9 is a novel innate antiviral factor against poxviruses.
SAMD9, an IFN-gamma (show IFNG Antibodies)-responsive protein, interacts with RGL2 (show RGL2 Antibodies) to diminish the expression of EGR1 (show EGR1 Antibodies), a protein of direct relevance to the pathogenesis of ectopic calcification and inflammation.
SAMD9 could be a key molecule to control cancer cell death by inactivated Sendai virus particle or IFN-beta (show IFNB1 Antibodies) treatment.
Mutation analysis revealed a homozygous mutation in the SAMD9 gene (K1495E), which was found to segregate with the disease in all families and to interfere with the protein expression.
This gene encodes a sterile alpha motif domain-containing protein. The encoded protein localizes to the cytoplasm and may play a role in regulating cell proliferation and apoptosis. Mutations in this gene are the cause of normophosphatemic familial tumoral calcinosis. Alternate splicing results in multiple transcript variants that encode the same protein.
sterile alpha motif domain-containing protein 9
, SAM domain-containing protein 9
, expressed in aggressive fibromatosis