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

Proline-serine-threonine phosphatase-interacting protein 2

Top mentioned proteins: BSA, ACID, STEP, HAD, Serum albumin
Papers on PSTPIP2
Long Lasting Microvascular Tone Alteration in Rat Offspring Exposed In Utero to Maternal Hyperglycaemia.
Fassot et al., Angers, France. In Plos One, Dec 2015
To evaluate the effect of maternal diabetes on fetal programming of vascular tone in offspring and its evolution during adulthood, we investigated vascular reactivity of third order mesenteric arteries from diabetic mother offspring (DMO) and control mother offspring (CMO) aged 3 and 18 months.
Suppressed expression of choline monooxygenase in sugar beet on the accumulation of glycine betaine.
Takabe et al., Nagoya, Japan. In Plant Physiol Biochem, Nov 2015
Choline monooxygenase (CMO) catalyzes the first step of the pathway and is believed to be a rate limiting step for GB synthesis.
PSTPIP2, a Protein Associated with Autoinflammatory Disease, Interacts with Inhibitory Enzymes SHIP1 and Csk.
Brdicka et al., Praha, Czech Republic. In J Immunol, Nov 2015
Mutations in the adaptor protein PSTPIP2 are the cause of the autoinflammatory disease chronic multifocal osteomyelitis in mice.
Increased neutrophil infiltration, IL-1 production and a SAPHO syndrome-like phenotype in PSTPIP2-deficient mice.
Hsu et al., Taipei, Taiwan. In Rheumatology (oxford), Jul 2015
OBJECTIVE: Proline-serine-threonine-phosphatase-interacting protein 2 (PSTPIP2) is involved in macrophage activation, neutrophil motility and osteoclast differentiation.
Divide and Conquer Approach to Contact Map Overlap Problem Using 2D-Pattern Mining of Protein Contact Networks.
Bhavani et al., In Ieee/acm Trans Comput Biol Bioinform, Jul 2015
A novel approach to Contact Map Overlap (CMO) problem is proposed using the two dimensional clusters present in the contact maps.
MorphoCol: An ontology-based knowledgebase for the characterisation of clinically significant bacterial colony morphologies.
Louren├žo et al., Braga, Portugal. In J Biomed Inform, Jun 2015
The Colony Morphology Ontology (CMO) is the first controlled vocabulary addressing the specificities of the morphology of clinically significant bacteria, whereas the MorphoCol publicly Web-accessible knowledgebase is an end-user means to search and compare CMO annotated colony morphotypes.
Diagnostic value of blood gene expression signatures in active tuberculosis in Thais: a pilot study.
Mahasirimongkol et al., Thailand. In Genes Immun, Jun 2015
FCGR1A, FCGR1B variant 1, FCGR1B variant 2, APOL1, GBP5, PSTPIP2, STAT1, KCNJ15, MAFB and KAZN had significantly higher expression level in active TB individuals as compared with healthy controls and previous TB cases (P<0.01).
Differential accumulation of glycinebetaine and choline monooxygenase in bladder hairs and lamina leaves of Atriplex gmelini under high salinity.
Takabe et al., Nagoya, Japan. In J Plant Physiol, Apr 2015
However, it remains unclear whether GB and its biosynthetic enzyme choline monooxygenase (CMO) accumulate in the bladder hairs.
Dietary modulation of the microbiome affects autoinflammatory disease.
Kanneganti et al., Memphis, United States. In Nature, 2015
Pstpip2(cmo) mice, which express a homozygous Leu98Pro missense mutation in the Pombe Cdc15 homology family protein PSTPIP2 (proline-serine-threonine phosphatase interacting protein 2), spontaneously develop osteomyelitis that resembles chronic recurrent multifocal osteomyelitis in humans.
Primed innate immunity leads to autoinflammatory disease in PSTPIP2-deficient cmo mice.
Stanley et al., United States. In Blood, 2009
PSTPIP2 deficiency leads to autoinflammatory disease.
"SAPHO syndrome and infections".
Trotta et al., Ferrara, Italy. In Autoimmun Rev, 2009
mutations are associated with spontaneous disease in mouse model of osteomyelitis
Chronic recurrent multifocal osteomyelitis: a concise review and genetic update.
Ferguson et al., Iowa City, United States. In Clin Orthop Relat Res, 2007
Indeed, mutations in LPIN2 cause a syndromic form of chronic recurrent multifocal osteomyelitis known as Majeed syndrome, while mutations in pstpip2 cause a murine form of the disorder.
Autoinflammatory bone disorders.
El-Shanti et al., Iowa City, United States. In Curr Opin Rheumatol, 2007
The genes responsible for Majeed syndrome (LPIN2), murine chronic multifocal osteomyelitis (pstpip2), and cherubism (SH3BP2 and possibly PTPN11) have been identified.
CYP17- and CYP11B-dependent steroid hydroxylases as drug development targets.
Bernhardt et al., Saarbr├╝cken, Germany. In Pharmacol Ther, 2006
Defects in steroid hydroxylating P450s are the cause of several severe defects such as the adrenogenital syndrome (AGS), corticosterone methyl oxidase (CMO) I or II deficiencies, or pseudohermaphroditism.
A missense mutation in pstpip2 is associated with the murine autoinflammatory disorder chronic multifocal osteomyelitis.
El-Shanti et al., Iowa City, United States. In Bone, 2006
A missense mutation in pstpip2 is associated with the autoinflammatory disorder chronic multifocal osteomyelitis.
The PCH family member MAYP/PSTPIP2 directly regulates F-actin bundling and enhances filopodia formation and motility in macrophages.
Stanley et al., United States. In Mol Biol Cell, 2005
MAYP directly regulates F-actin bundling and enhances filopodia formation and motility in macrophages.
Molecular genetic study in two patients with congenital hypoaldosteronism (types I and II) in relation to previously published hormonal studies.
Sippell et al., Germany. In Eur J Endocrinol, 1998
According to the nomenclature proposed by Ulick, the defects are termed corticosterone methyl oxidase (CMO) deficiency type II in patient 1, and type I in patient 2 respectively.
Mutations in human 11 beta-hydroxylase genes: 11 beta-hydroxylase deficiency in Jews of Morocco and corticosterone methyl-oxidase II deficiency in Jews of Iran.
White et al., Jerusalem, Israel. In J Steroid Biochem Mol Biol, 1993
CYP11B1 encodes a specific cytochrome P-450 (P-450c11) necessary for cortisol biosynthesis, with predominantly 11 beta-hydroxylase and moderate 18-hydroxylase activity, whereas CYP11B2 encodes another isozyme (P-450cmo) necessary for aldosterone biosynthesis, with 11 beta-hydroxylase, 18-hydroxylase and 18-oxidase activities (the latter two termed corticosterone methyl-oxidase I and II; CMO-I and II, respectively).
An inherited defect in aldosterone biosynthesis caused by a mutation in or near the gene for steroid 11-hydroxylase.
White et al., New York City, United States. In N Engl J Med, 1988
The final step in aldosterone biosynthesis, an oxidation at position 18 of 18-hydroxycorticosterone, is catalyzed by an enzymatic activity termed corticosterone methyl oxidase II (CMO II).
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