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Solute carrier family 20

Pit2, Ram-1, GLVR-2
This gene encodes a member of the inorganic phosphate transporter family. The encoded protein is a type 3 sodium-dependent phosphate symporter that plays an important role in phosphate homeostasis by mediating cellular phosphate uptake. The encoded protein also confers susceptibility to viral infection as a gamma-retroviral receptor. Mutations in this gene may play a role in familial idiopathic basal ganglia calcification. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene. [provided by RefSeq, Mar 2012] (from NCBI)
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Top mentioned proteins: Pit-1, CAN, ACID, HAD, SLC34A2
Papers on Pit2
Slc20a2 is critical for maintaining a physiologic inorganic phosphate level in cerebrospinal fluid.
Pedersen et al., Århus, Denmark. In Neurogenetics, Jan 2016
UNASSIGNED: Mutations in the SLC20A2-gene encoding the inorganic phosphate (Pi) transporter PiT2 can explain approximately 40 % of the familial cases of the rare neurodegenerative disorder primary familial brain calcification (Fahr's disease).
Familial idiopathic basal ganglia calcification: Histopathologic features of an autopsied patient with an SLC20A2 mutation.
Kakita et al., Niigata, Japan. In Neuropathology, Jan 2016
Immunohistochemistry using an antibody against type III sodium-dependent phosphate transporter 2 (PiT-2), the SLC20A2 product, demonstrated that astrocytic processes were labeled in several regions in control brains, whereas in the patient, reactivity in astrocytes was apparently weak.
Update and Mutational Analysis of SLC20A2: A Major Cause of Primary Familial Brain Calcification.
Oliveira et al., Recife, Brazil. In Hum Mutat, May 2015
SLC20A2 encodes an inorganic phosphate transporter, PiT-2, widely expressed in various tissues, including brain, and is part of a major family of solute carrier membrane transporters.
Primary familial brain calcification: update on molecular genetics.
Federico et al., Siena, Italy. In Neurol Sci, May 2015
SLC20A2 gene codes for the 'sodium-dependent phosphate transporter 2' (PiT-2), a cell membrane transporters of inorganic phosphate, involved in Pi uptake by cells and maintenance of Pi body levels.
First report of a de novo mutation at SLC20A2 in a patient with brain calcification.
Oliveira et al., Recife, Brazil. In J Mol Neurosci, 2014
Mutations in the SLC20A2 gene account for ~40% of inherited cases, and this gene encodes an inorganic phosphate transporter (PiT-2), a transmembrane protein associated with Pi homeostasis.
Deregulated Renal Calcium and Phosphate Transport during Experimental Kidney Failure.
NIGRAM Consortium et al., Nijmegen, Netherlands. In Plos One, 2014
Furthermore, kidney failure was characterized by enhanced renal expression of the transient receptor potential cation channel subfamily V member 5 (TRPV5), calbindin-D28k, and sodium-dependent Pi transporter type 2b (NaPi2b), whereas the renal expression of sodium-dependent Pi transporter type 2a (NaPi2a) and type 3 (PIT2) were reduced.
The genetics of primary familial brain calcifications.
Klein et al., Lübeck, Germany. In Curr Neurol Neurosci Rep, 2014
In the past 2 years, 3 genes have been identified to cause PFBC, (ie, SLC20A2, PDGFRB, and PDGFB).
Genetic diseases of renal phosphate handling.
Hernando et al., Zürich, Switzerland. In Nephrol Dial Transplant, 2014
At least three transport proteins are responsible for renal phosphate reabsorption: NAPI-IIa (SLC34A1), NAPI-IIc (SLC34A3) and PIT-2 (SLC20A2).
Comparing the expression patterns of placental magnesium/phosphorus-transporting channels between healthy and preeclamptic pregnancies.
Jeung et al., Ch'ŏngju, South Korea. In Mol Reprod Dev, 2014
The expression of MPC genes (TRPM6, TRPM7, PiT-1, and PiT-2) was down-regulated in preeclamptic placenta tissues during preterm labor, and generally remained lower at term labor-although TRPM7 expression in the central placenta or PiT-2 expression in whole placenta was unchanged or up-regulated.
Active removal of inorganic phosphate from cerebrospinal fluid by the choroid plexus.
Renfro et al., Faro, Portugal. In Am J Physiol Renal Physiol, 2014
RT-PCR revealed both P(i) transporter (PiT)1 and PiT2 (SLC20 family) gene expression, but no Na(+)-P(i) cotransporter II (SLC34 family) expression, in the shark CP.
Renal-specific and inducible depletion of NaPi-IIc/Slc34a3, the cotransporter mutated in HHRH, does not affect phosphate or calcium homeostasis in mice.
Hernando et al., Zürich, Switzerland. In Am J Physiol Renal Physiol, 2014
The proximal renal epithelia express three different Na-dependent inorganic phosphate (Pi) cotransporters: NaPi-IIa/SLC34A1, NaPi-IIc/SLC34A3, and PiT2/SLC20A2.
Highly efficient tumor transduction and antitumor efficacy in experimental human malignant mesothelioma using replicating gibbon ape leukemia virus.
Kasahara et al., Nishinomiya, Japan. In Cancer Gene Ther, 2013
Quantitative reverse transcription PCR demonstrated that ACC-MESO-1 cells express higher PiT-1 (GALV receptor) and lower PiT-2 (AMLV receptor) compared with normal mesothelial cells and other mesothelioma cells, presumably accounting for the distinctive finding that GALV-RRV replicates much more robustly than AMLV-RRV in these cells.
[The causative gene of Parkinsonism and its medical treatment strategy].
Inden, Gifu, Japan. In Yakugaku Zasshi, 2013
Type-III sodium-dependent phosphate transporter 2 (PiT-2), the protein encoded by SLC20A2, plays an important role in phosphate homeostasis.
An update on primary familial brain calcification.
Oliveira et al., Santiago de Compostela, Spain. In Int Rev Neurobiol, 2012
Recently, mutations in the SLC20A2 gene coding for the inorganic phosphate transporter PiT2 were linked to PFBC, thereby implicating impaired phosphate transport as an underlying disease mechanism.
Mutations in SLC20A2 link familial idiopathic basal ganglia calcification with phosphate homeostasis.
Liu et al., Wuhan, China. In Nat Genet, 2012
Mutations in SLC20A2 link familial idiopathic basal ganglia calcification with phosphate homeostasis.
Hypophosphatemia in vitamin D receptor null mice: effect of rescue diet on the developmental changes in renal Na+ -dependent phosphate cotransporters.
Miyamoto et al., Tokushima, Japan. In Pflugers Arch, 2011
reduced intestinal Pi absorption in VDR (-/-) mice does not seem to be the only factor that causes hypophosphatemia; reduced Npt2a, Npt2c, or PiT-2 protein levels during development might also cause hypophosphatemia and rickets in VDR (-/-) mice.
Mapping of the minimal inorganic phosphate transporting unit of human PiT2 suggests a structure universal to PiT-related proteins from all kingdoms of life.
Pedersen et al., Århus, Denmark. In Bmc Biochem, 2010
the human PiT2 histidine, H(502), and the human PiT1 glutamate, E(70),--both conserved in eukaryotic PiT family members--are critical for P(i) transport function
Acute parathyroid hormone differentially regulates renal brush border membrane phosphate cotransporters.
Wagner et al., Zürich, Switzerland. In Pflugers Arch, 2010
expression in renal brush border reduced by parathyroid hormone
Compensatory regulation of the sodium/phosphate cotransporters NaPi-IIc (SCL34A3) and Pit-2 (SLC20A2) during Pi deprivation and acidosis.
Sorribas et al., Zaragoza, Spain. In Pflugers Arch, 2010
Results describe the regulation of the sodium/phosphate cotransporters SCL34A3 and SLC20A2 during phosphate deprivation and acidosis in rat kidney.
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