anti-Protein tyrosine Phosphatase, Non-Receptor Type 5 (Striatum-Enriched) (PTPN5) Antibodies

Mouse (Murine) Protein tyrosine Phosphatase, Non-Receptor Type 5 (Striatum-Enriched) (PTPN5) interaction partners

1. STEP61 undergoes proteolytic degradation in conditions leading to synaptic strengthening and memory formation

2. activation of synaptic NMDAR by bicuculline or D-serine results in the ubiquitination and proteasomal degradation of STEP61, and increased surface localization of GluN1/GluN2B receptors.

3. STEP plays an important role at nerve terminals in the regulation of Ca(2+) homeostasis and neurotransmitter release.

4. STEP61 degradation is an important event in BDNF-mediated effects.

5. STEP has a key role in the regulation of psychomotor action and physical dependency to morphine. These data suggest that STEP inhibition may be a critical target for the treatment of withdrawal symptoms associated with morphine.

6. This study demonistrated that behavioral, molecular, and electrophysiological data indicate that spinal STEP61 plays a regulatory role in nociception.

7. STEP61 regulates BDNF expression, with implications for cognitive functioning in CNS disorders.

8. The study provides further insight into the mechanisms of regulation of STEP61 and also offers a molecular basis for the Zn(2+)-induced sustained activation of ERK2.

9. STEP contributes, at least in part, to the protection against the ingestion of aversive agents.

10. These results indicate that STEP61 is a novel substrate of parkin, although further studies are necessary to determine whether elevated STEP61 levels directly contribute to the pathophysiology of PD.

11. Abeta regulating STEP61 activity is mediated by Abeta binding to alpha7 nAChRs

12. Increased STEP and calpain activation contribute to altered NMDAR localization in an Huntington's disease mouse model.

13. genetically reducing STEP significantly diminishes seizures and restores select social and nonsocial anxiety-related behaviors in Fmr1(KO) mice

14. the first study to identify Pyk2 as a substrate for STEP.

15. Increased STEP61 plays a role in amyloid Abeta-mediated internalization of the (AMPAR) subunits GluA1/GluA2 (formerly GluR1/GluR2).

16. The absence of STEP improves cognitive performance, and may do so by the regulation of downstream effectors necessary for synaptic transmission.

17. STEP pathway is severely downregulated in the presence of mutant huntingtin and may participate in compensatory mechanisms activated by striatal neurons that lead to resistance to excitotoxicity.

18. STEP may be required for ethanol's amnesic effects.

19. Electrical stimulation of the hippocampal-entorhinal cortex pathway in STEP knockout mice resulted in less activation of the dentate gyrus granule cell layer (GCL), but greater activation of the hilus in STEP knockouts, compared with heterozygous slices.

20. genetic manipulations to reduce STEP activity in a triple transgenic AD mouse model and show that a decrease in STEP levels reverses cognitive and cellular deficits observed in these mice.

Human Protein tyrosine Phosphatase, Non-Receptor Type 5 (Striatum-Enriched) (PTPN5) interaction partners

1. validated the functional importance of an identified interaction network by characterizing a distinct novel interaction between PTPN5 and Mob1a.

2. This current study demonstrated that spinal STEP61 regulated LTP of C fiber-evoked field potentials, one of the extensively studied cellular models of central sensitization.

3. a dual role for PSD-95 in stabilizing synaptic NMDARs by binding directly to GluN2B but also by promoting synaptic exclusion and degradation of the negative regulator STEP61.

4. STEP is involved in the mechanism of depressive disorders and it is a promising molecular target for atypical antidepressant drugs of new generation. (Review)

5. Data suggest that PP5/PTPN5 is overexpressed in liver samples from patients with hepatocellular carcinoma (HCC); overexpression of PP5/PTPN5 appears to correlate with tumor burden/stage. Inhibition of PP5/PTPN5 suppresses proliferation and promotes apoptosis of HCC cells; inhibition of PP5/PTPN5 involves activation of AMPK.

6. A rare missense variant in the PTPN5 gene (rs56234898; minor allele frequency 1.5%) was significantly associated with decreased severity of Post-Burn Hypertrophic Scarring(P = 1.3x10-6).

7. STEP levels are unchanged in pre-frontal cortex and associative striatum in post-mortem human brain samples from subjects with schizophrenia, bipolar disorder and major depressive disorder

8. Article focuses on the most recent findings on STEP, discuss how STEP expression and activity are maintained during normal cognitive function, and how disruptions in STEP activity contribute to a number of illnesses. [Review]

9. Decreased STEP protein activation in corpus striatum contributes to early enhanced apoptotic signaling in YAC model transgenic mice.

10. This experiments demonstrated that deletion of STEP can enhance experience-induced neuroplasticity and memory formation

11. The results imply a model in which PTPN5 may play a role in normal cognitive functioning and contribute to aspects of the neuropathology of schizophrenia.

12. This study identified a novel role for PTPN5 in mediating the development of stress-related cognitive and morphological changes.

13. STEP(61kDa) is required for Abeta transgene-mediated internalization of GluA1/GluA2 glutamate receptors in a transgenic mousemodel.

14. STEP contributes to aspects of the pathophysiology in Alzheimer's disease; loss of GluN1/GluN2B subunits from neuronal membranes and Abeta-mediated NMDAR internalization are discussed

15. findings show that STEP(61) levels are progressively increased in the prefrontal cortex of Alzheimer disease brains

16. determined high-resolution structures of all of the human family members of Mitogen-Activated Protein Kinase-specific protein tyrosine phosphatases

17. in colorectal tumors, microsatellite repeats mutation rates are higher than the mean mutation frequency