prostatic

Prostatic Acid Phosphatase (PAP) belongs to the histidine acid phosphatase family. PAP can catalyze the hydrolysis of member of phosphate monoestyers, including phosphorylated protein. PAP can high expression in metastasized prostate cancer, moderately expression level in bone diseases, blood cell disease, and the concentration of PAP is used to monitor and assess the proession of prostate cancer. The optimum PH of PAP is from 4 to 6; its activity can be inhibited by L(+)-tartrate.

Serine protease inhibitor which exhibits anti-trypsin activity. In the pancreas, protects against trypsin-catalyzed premature activation of zymogens.; In the male reproductive tract, binds to sperm heads where it modulates sperm capacitance by inhibiting calcium uptake and nitrogen oxide (NO) production. SPINK1 Protein, Mouse, Recombinant (His) is expressed in yeast with N-6xHis tag. The predicted molecular weight is 8.1 kDa and the accession number is P09036.

Prostatic Acid Phosphatase Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 42 kDa and the accession number is Q8CE08-1.

Prostatic Acid Phosphatase Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 42 kDa and the accession number is P15309-2.

IL-17RC (interleukin-17 receptor-like) gene codes for a transmembrane protein, the full length of which inhibits apoptosis in prostate cancer cells. IL-17RC gene transcribes over a dozen different splice variants of mRNA. IL-17RC protein isoforms are differentially expressed in prostatic cells and cancer tissues and may play a negative or positive role in the initiation and progression of prostate cancer.

Secretagogin, also known as SCGN, is a secreted protein that is detectable in human serum after ischemic neuronal damage. It is a recently described calcium-binding protein. Secretagogin SCGN is expressed at high levels in the pancreatic islets of Langerhans and to a much lesser extent in the gastrointestinal tract (stomach, small intestine and colon), the adrenal medulla and cortex and the thyroid C-cells. In the brain, the expression of Secretagogin SCGN is restricted to distinct subtypes of neurons with highest expression in the molecular layer of the cerebellum (stellate and basket cells), in the anterior part of the pituitary gland, in the thalamus, in the hypothalamus and in a subgroup of neocortical neurons. Secretagogin SCGN is widely expressed in prostatic adenocarcinoma as opposed to adenocarcinomas in other organs. The function of Secretagogin SCGN is unknown, but it has been suggested in beta-cells to influence calcium-influx and has been observed downregulated in diabetes-prone BB rat islets exposed to cytokines. Secretagogin SCGN is involved in the calcium metabolism of tumour cells and endothelial cells in a subset of neoplasms of the brain and its coverings. Secretagogin SCGN is also a novel marker for neuroendocrine differentiation.

Glutamate decarboxylase 1, also known as 67 kDa glutamic acid decarboxylase, Glutamate decarboxylase 67 kDa isoform and GAD1, is a member of thegroup II decarboxylase family. GAD1 is expressed in benign and malignant prostatic tissue and may serve as a highly prostate-specific tissue biomarker. GAD1 isoform3 is expressed in pancreatic islets, testis, adrenal cortex, and perhaps other endocrine tissues, but not in brain. Tissue-specific markers are useful for identification of tumour type in advanced cancers of unknown origin. In plants, as in most eukaryotes, glutamate decarboxylase catalyses the synthesis of GABA. Root-specific calcium calmodulin-regulated GAD1 plays a major role in GABA synthesis in plants under normal growth conditions and in response to stress. Defects in GAD1 are the cause of cerebral palsy spastic quadriplegic type 1 (CPSQ1)which is a non-progressive disorder of movement and or posture resulting from defects in the developing central nervous system. Affected individuals manifest symmetrical, non-progressive spasticity and no adverse perinatal history or obvious underlying alternative diagnosis.