渗透性应激PCR基因芯片Osmotic Stress PCR Array

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Osmotic Stress PCR Array

渗透性应激PCR基因芯片
 

Product	Species	Technology	Cat. No.
Osmotic Stress PCR Array	Human	Gene Expression	PAHS-151Z
Osmotic Stress PCR Array	Mouse	Gene Expression	PAMM-151Z
Osmotic Stress PCR Array	Rat	Gene Expression	PARN-151Z

The Human Osmotic Stress RT² Profiler PCR Array profiles the expression of 84 key genes involved in the cellular response to changes in osmolarity. Under normal physiological conditions, the majority of mammalian cells grow within an isotonic environment. The renal medulla, one exception to this rule, experiences not only high osmolarity during urine concentration (>10-fold normal levels), but also a broad range of potential salt concentrations at any given time. Osmolarity changes affect the expression of hundreds of genes driven by the key transcription factor TonEBP/OREBP (NFAT5). During osmotic stress, expression of water transporters, ion transport genes, and protein chaperones increases. Cells also undergo cytoskeletal rearrangement. Other typical cellular effects include oxidative stress, cell cycle arrest, transcription/translation arrest, and mitochondrial depolarization, all of which can result in DNA damage and apoptosis. In cellular systems other than the kidney medulla, a general electrolyte imbalance can lead to chronic hyponatremia and central pontine myelinolysis, a rare disease occurring in the central nervous system and involving some of the same transporters commonly expressed in the kidney medulla. This array includes molecular transporters, direct NFAT5 targets, and hormones and receptors involved in the hyperosmotic response. Genes whose expression is commonly altered during osmotic stress are also included. Using real-time PCR, research studies can easily and reliably analyze the expression of a focused panel of genes involved in osmotic stress with this array.
人类的渗透性应激PCR基因芯片可用于研究参与细胞渗透性应激的84个关键基因的表达。正常的生理条件下，大多数哺乳动物细胞在等渗透压的环境中生存。渗透压的变化会影响多基因的表达。在渗透性应激中，水转运体、离子转运基因和蛋白质的分子伴侣的表达都有增加，细胞也经历了细胞骨架的重排。其他典型的细胞的影响还包括：氧化应激，细胞周期阻滞，转录/翻译暂停，线粒体去极化等，从而导致DNA损伤和细胞凋亡。除肾髓质外的其他细胞体系中，电解质紊乱可导致慢性低钠血症和脑桥ZY髓鞘溶解症（一种罕见的发生在神经系统的疾病），并涉及一些通常在肾髓质中表达的转运体。该芯片包括分子转运，NFAT5直接下游基因，参与高渗反应的激素及其受体，及其他再渗透性应激中有变化的基因。利用实时定量PCR，研究者可以方便并且可信地研究与渗透性应激有关的基因的表达。
Transport:
Water Transporters:AQP1, AQP2, AQP3, AQP4, AQP5, AQP9.
Ion Channels:CFTR, KCNJ1, MLC1, TRPV4.
Other Transporters:ABCB1 (MDR1), ATP1A1, ATP1B1, LCN2 (NGAL), SLC14A2, SLC2A1, SLC38A2, SLC5A3, SLC6A12, SLC6A6, SLC9A2, SLC9A3.
TonEBP/OREBP (NFAT5) Targets:AQP2, SLC14A2, SLC5A3, SLC6A12, SLC6A6.
Hormones & Receptors:ADM, AGT, AGTR1, AVP, EDN1, GUCA2A, INS, NPR1, OXT.
Molecular Chaperones:CALR, CRYAB, HSP90AA1, HSPA1A, HSPA4 (HSP70), HSPA4 (HSP70), HSPA4L (OSP94), HSPA5 (GRP78), HSPB1 (HSP27).
DNA Damage:DDIT3 (GADD153/CHOP), GADD45A, GADD45B, GADD45G, HMOX1, MAPK1 (ERK2), TP53.
Oxidative Stress:CRYAB, DDIT3 (GADD153/CHOP), DUSP1 (PTPN16), EGFR, FOS, HMOX1, NOS3, JUN, TAT, TPM4.
Regulation of Translation:AKT1, CALR, HSPB1 (HSP27), MAPK1 (ERK2), ZFP36L1.
Mitochondrial Organization:AKT1, HSP90AA1, HSPA4 (HSP70), JUN, MAP3K1 (MEKK1), NOS3, PCK2, TP53.
Cytoskeleton Organization:CALR, CRYAB, EDN1, MAP3K1 (MEKK1), PTK2, VIM.
Apoptosis:AKT1, IL1B, MAPK8 (JNK1), NFKBIA (IκBa/MAD3), PAK2, SGK1, VEGFA.
Cell Cycle:AKT1, IL1B.
Adhesion:AGT, CD9, CTGF, EGFR, IL1B, IL8, ITGB1, TNF.
Transcription Factors:AKR1B1 (NFAT5), ATF4, DDIT3 (GADD153/CHOP), EGR1, EGR3, FOS, JUN, NFAT5, PAX2, SNAI1, TP53, ZFP36L1.
Others:LTB, MAP2K2 (MEK2), ODC1, PDIA4, PLAT (tPA), SRC, TGFA