Disease relevance of Phgdh

• Using Western blotting with ZF5 and sera of autoimmune disease, we detected one serum, named M6 serum, which contains the antibody against a transcriptional repressor ZF5 [1].
• Sera from pigs naturally infected with B. hyodysenteriae also reacted with recombinant BmpB expressed in E. coli [2].
• This phenomenon was demonstrated in lymphocytes and lymphoma cells treated with anti-H-2 sera; spleen lymphocytes treated with concanavalin A or anti-immunoglobulin antibodies, and VSV-infected mouse fibroblast line MC57 treated with antiserum against viral antigens [3].
• Antiserum raised against PKF and sera from rabbits bearing rous sarcoma virus (RSV)-induced tumors quantitatively precipitate the same 60 kd phosphoprotein from cell lysates of three different RSV-transformed cell lines [4].
• BPAG1 is the major antigenic determinant of autoimmune sera of bullous pemphigoid (BP) patients [5].

Psychiatry related information on Phgdh

• Sera from mice with 8-wk Schistosoma mansoni infection, chronic (20-wk infection) moderate splenomegaly syndrome (MSS), or chronic hypersplenomegaly syndrome (HSS) were passed over an S. mansoni soluble egg antigen (SEA) immunoaffinity column to prepare Ids (8WkId, MSS Id, HSS Id) [6].
• The latency period before the original paraprotein was detected in the sera of recipients varied in different experiments between 1 and 9 months after transplantation [7].

High impact information on Phgdh

• Antibodies to DNA and nucleoproteins are found in sera of individuals with systemic autoimmune disease [8].
• In addition deficient mice produce antibody to mouse C5 when injected with sera from C5 sufficient (normal) strains [9].
• Mouse T-cell surface glycoprotein recognised by heterologous anti-thymocyte sera and its relationship to Thy-1 antigen [10].
• Thymus reactive IgM autoantibodies in normal mouse sera [11].
• This mechanism is dependent on the signaling pathway intermediary myeloid differentiation factor 88 (MyD88), such that neither IL-1R nor MyD88-deficient mice developed visually detectable synovitis after transfer of arthritogenic sera [12].

Chemical compound and disease context of Phgdh

• The tumor necrosis-inducing factor (TNF) found in sera of Corynebacterium parvum-treated, endotoxin-stressed BALB/C and outbred albino CD-1 mice has been purified to a single band of protein by polyacrylamide gel electrophoresis after identification and removal of contaminating albumin and transferrin [13].
• The tyrosine-specific protein kinase activity previously described in T-antigens of polyoma virus immunoprecipitated with anti-tumour sera has been investigated using monoclonal antibodies [14].
• Molecular differences between dopamine (DA) neurons may explain why the mesostriatal DA neurons in the A9 region preferentially degenerate in Parkinson's disease (PD) and toxic models, whereas the adjacent A10 region mesolimbic and mesocortical DA neurons are relatively spared [15].
• Little or no precipitation of purified Rauscher murine leukemia virus Mr 70,000 glycoprotein was observed with sera of mice immunized with P815 cells [16].
• First, we assessed the neutralizing potential of these antibodies in C57BL/6 mice under acute septic shock by measuring IL-1beta in sera 4 h after lipopolysaccharide injection [17].

Biological context of Phgdh

• In the cerebral cortex of transgenic mouse embryos, the Phgdh promoter-LacZ transgene DNA containing -1,794/+4 promoter sequences directed beta-galactosidase (beta-Gal) expression mainly to Phgdh-positive neuroepithelium and radial glia [18].
• Transient transfection analysis revealed that the cis-acting elements necessary for basal transcription of Phgdh are contained within the -196/+4 proximal sequence of the promoter, in which the conserved Sp1 recognition sites play an important role for basal promoter activity [19].
• Although basal promoter activity of the gene appeared to depend on an Sp1 binding sequence residing between -193 and -184 in both glial and neuronal cultures, an upstream 5'-flanking region between -1,794 and -1,095 contributed to up-regulation of Phgdh transcription in a glial-cell-specific manner [18].
• These observations suggest the presence of cis-acting elements that confer the cell type specificity of Phgdh transcription in the distal promoter region [18].
• Structural analysis demonstrated that the Phgdh gene spans approximately 27 kilobases (kb) in length and comprises 12 exons with 11 intervening introns [19].

Anatomical context of Phgdh

• Phgdh is expressed exclusively by neuroepithelium and radial glia in developing brain and later mainly by astrocytes [18].
• To determine the physiological importance of Phgdh-dependent L-serine biosynthesis in vivo, we generated Phgdh-deficient mice using targeted gene disruption in embryonic stem cells [20].
• 5. Striking abnormalities were evident in the central nervous system in which the Phgdh null mutation culminated in hypoplasia of the telencephalon, diencephalon, and mesencephalon; in particular, the olfactory bulbs, ganglionic eminence, and cerebellum appeared as indistinct structures [20].
• The majority of sera from acute and chronic active EAE animals displayed intense labelling of astrocytes and only weak staining of oligodendrocytes when tested on sections of normal guinea pig brain tissue [21].
• Some of these cloned cell lines bound anti-GFAP sera and therefore appeared to be astrocytic [22].

Associations of Phgdh with chemical compounds

• D-3-Phosphoglycerate dehydrogenase (Phgdh; EC 1.1.1.95) is a necessary enzyme for de novo L-serine biosynthesis via the phosphorylated pathway [18].
• The original activity was not restored readily by in vitro treatment of the sera with pyridoxal phosphate (PLP), in contrast to the rapid activation, by the same treatment, of apoAAT in the sera from control mice [23].
• Sera of deficient mice lack detectable C5 activity and protein2,3 [9].
• We found significantly increased amounts of both cytokines in the sera of CB3/LPS-treated mice compared with animals treated only with LPS [24].
• Immunoprecipitation and polyacrylamide gel electrophoresis analysis of the molecules reactive with anti-Qa-1 and anti-37 sera show that the Qa-1 molecule of Qa-1b (Qa-1.2) mouse strains is identical to the product of gene 37 on the basis of molecular weight, pI, and strain distribution [25].

Regulatory relationships of Phgdh

• In addition, 3PGDH was highly expressed throughout development in the olfactory ensheathing glia, a specialized supporting cell that thoroughly ensheathes olfactory nerves [26].

Other interactions of Phgdh

• Anti-MBP and anti-GFAP, isotypes IgM and IgG, were measured in sera by ELISA on day 38 [27].
• The preferential glial expression of ASCT1 was consistent with that of 3PGDH, and their extensive colocalization was demonstrated at the cellular level [28].
• At early stages when the neural wall consists exclusively of the ventricular zone, neuroepithelial stem cells expressed 3PGDH strongly and homogeneously [26].

Analytical, diagnostic and therapeutic context of Phgdh

• Specificity of the antibodies was established by immunoblotting against sera and brain homogenates of wild type and apoE-deficient mice [29].
• To investigate whether such a metabolic neuron-glial relationship is fundamental to the developing and adult brain, we examined by in situ hybridization and immunohistochemistry the cellular expression of 3-phosphoglycerate dehydrogenase (3PGDH), the initial step enzyme for de novo l-serine biosynthesis in animal cells [26].
• A clone with little H-2Dd (10-15% lysable) was tumorigenic even after treatment with anti-H-2Dd sera; at least 50% of the tumor cells were lysed by anti-H-2Dd [30].
• Analysis by immunoprecipitation shows that the viral capsid protein is part of the active nucleoprotein complex, but recognition of the complex by only a subset of anti-capsid sera implies that the protein is constrained conformationally [31].
• Examination of sera from infected mice revealed autoantibodies that, by immunofluorescence, reacted with cytoplasmic antigens in the islets of Langerhans, anterior pituitary, and gastric mucosa of uninfected mice [32].

References