Western Blot: 1: 500- 1: 1,000 ELISA: Propose dilution 1: 10,000 Determining optimal working dilutions by titration test.
Beschränkungen
Nur für Forschungszwecke einsetzbar
Lagerung
-20 °C
Irving, Bamford: "Role of mitogen- and stress-activated kinases in ischemic injury." in: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, Vol. 22, Issue 6, pp. 631-47, (2002) (PubMed).
Cuenda: "Mitogen-activated protein kinase kinase 4 (MKK4)." in: The international journal of biochemistry & cell biology, Vol. 32, Issue 6, pp. 581-7, (2000) (PubMed).
Kuan, Yang, Samanta Roy, Davis, Rakic, Flavell: "The Jnk1 and Jnk2 protein kinases are required for regional specific apoptosis during early brain development." in: Neuron, Vol. 22, Issue 4, pp. 667-76, (1999) (PubMed).
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Forsgren, Moravec, Moravec: "Catecholamine-synthesizing enzymes and neuropeptides in rat heart epicardial ganglia; an immunohistochemical study." in: The Histochemical journal, Vol. 22, Issue 12, pp. 667-76, (1991) (PubMed).
Target
MAPK10
(Mitogen-Activated Protein Kinase 10 (MAPK10))
MAPK10 (mitogen-activated protein kinase 10 ), also called JNK3, which is located on chromosome 4q22.1q23, JNK is an important contributor to stress-induced apoptosis, its isoforms (JNK1, JNK2, and JNK3) have distinct roles in cerebral ischemia. JNK1 is the major isoformresponsible for the high level of basal JNK activity in the brain. In contrast, targeted deletion of Jnk3 not only reduces the stress-induced JNK activity, but also protects mice from brain injury after cerebral ischemiahypoxia. The downstream mechanism of JNK3-mediated apoptosis include the induction of Bim and Fas and the mitochondrial release of cytochrome c. which suggest that JNK3 is a potential target for neuroprotection therapies in stroke. JNK3 is crucial for neuronal apoptosis (stress-induced) and selectively expressed in the nervous system and heart.