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Die folgenden MAPmates™ sollten nicht zusammen analysiert werden: -MAPmates™, die einen unterschiedlichen Assaypuffer erfordern. -Phosphospezifische und MAPmate™ Gesamtkombinationen wie Gesamt-GSK3β und Gesamt-GSK3β (Ser 9). -PanTyr und locusspezifische MAPmates™, z.B. Phospho-EGF-Rezeptor und Phospho-STAT1 (Tyr701). -Mehr als 1 Phospho-MAPmate™ für ein einziges Target (Akt, STAT3). -GAPDH und β-Tubulin können nicht mit Kits oder MAPmates™, die panTyr enthalten, analysiert werden.
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48-602MAG
Buffer Detection Kit for Magnetic Beads
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This Anti-phospho JAK-2 (Tyr570) Antibody is validated for use in WB, WB, WB for the detection of phospho JAK-2 (Tyr570).
More>>This Anti-phospho JAK-2 (Tyr570) Antibody is validated for use in WB, WB, WB for the detection of phospho JAK-2 (Tyr570). Less<<
Anti-phospho JAK-2 (Tyr570) Antibody: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
JAK-2 (Janus Kinase 2) belongs to the emerging family of non-receptor Janus tyrosine kinases, which regulate a spectrum of cellular functions downstream of activated cytokine receptors in the lympho-hematopoietic system. Immunological stimuli, such as interferons and cytokines, induce recruitment of Stat transcription factors to cytokine receptor-associated JAK-2. JAK-2 then phosphorylates proximal Stat factors, which subsequently dimerize, translocate to the nucleus and bind to CIS elements upstream of target gene promoters to regulate transcription. The canonical JAK/Stat pathway is integral to maintaining a normal immune system by stimulating proliferation, differentiation, survival and host resistance to pathogens. Altering JAK/Stat signaling to reduce cytokine induced pro-inflammatory responses represents an attractive target for anti-inflammatory therapies. Within the JAK-2 kinase domain, there is a region that has considerable sequence homology to the regulatory region of the insulin receptor.
References
Product Information
Format
Affinity Purified
Control
Transfected HEK293T cell lysates
Presentation
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4, 150 mM NaCl) with 0.05% sodium azide.
This gene product is a protein tyrosine kinase involved in a specific subset of cytokine receptor signaling pathways. It has been found to be constituitively associated with the prolactin receptor and is required for responses to gamma interferon. Mice that do not express an active protein for this gene exhibit embryonic lethality associated with the absence of definitive erythropoiesis. [provided by RefSeq].
FUNCTION:Plays a role in leptin signaling and control of body weight By similarity. Tyrosine kinase of the non-receptor type, involved in interleukin-3 and probably interleukin-23 signal transduction.
CATALYTIC ACTIVITY:ATP + a [protein]-L-tyrosine = ADP + a [protein]-L-tyrosine phosphate.
SUBUNIT STRUCTURE: Interacts with SIRPA and SH2B1 By similarity. Interacts with IL23R, SKB1 and STAM2.
SUBCELLULAR LOCATION: Endomembrane system; Peripheral membrane protein By similarity. Note: Wholly intracellular, possibly membrane associated By similarity.
TISSUE SPECIFICITY: Expressed in blood, bone marrow and lymph node.
DOMAIN: Possesses two phosphotransferase domains. The second one probably contains the catalytic domain By similarity, while the presence of slight differences suggest a different role for domain 1.
PTM:Leptin promotes phosphorylation on tyrosine residues, including phosphorylation on Tyr-813 by similarity.
INVOLVEMENT IN DISEASE: Chromosomal aberrations involving JAK2 are found in both chronic and acute forms of eosinophilic, lymphoblastic and myeloid leukemia. Translocation t(8;9)(p22;p24) with PCM1 links the protein kinase domain of JAK2 to the major portion of PCM1. Translocation t(9;12)(p24;p13) with ETV6.Defects in JAK2 are a cause of susceptibility to Budd-Chiari syndrome [MIM:600880]. Budd-Chiari syndrome is a spectrum of disease states, including anatomic abnormalities and hypercoagulable disorders, resulting in hepatic venous outflow occlusion. Clinical manifestations observed in the majority of patients include hepatomegaly, right upper quadrant pain, and abdominal ascites.
Defects in JAK2 are associated with polycythemia vera (PV) [MIM:263300]. PV, the most common form of primary polycythemia, is caused by somatic mutation in a single hematopoietic stem cell leading to clonal hematopoiesis. PV is a myeloproliferative disorder characterized predominantly by erythroid hyperplasia, but also by myeloid leukocytosis, thrombocytosis, and splenomegaly. Familial cases of PV are very rare and usually manifest in elderly patients.
Defects in JAK2 gene may be a cause of essential thrombocythemia (ET) [MIM:187950]. ET is characterized by elevated platelet levels due to sustained proliferation of megakaryocytes, and frequently lead to thrombotic and haemorrhagic complications.
Defects in JAK2 are associated with familial myelofibrosis [MIM:254450]. Myelofibrosis with myeloid metaplasia is a myeloproliferative disease with annual incidence of 0.5-1.5 cases per 100,000 individuals and age at diagnosis around 60 (an increased prevalence is noted in Ashkenazi Jews). Clinical manifestations depend on the type of blood cell affected and may include anemia, pallor, splenomegaly, hypermetabolic state, petechiae, ecchymosis, bleeding, lymphadenopathy, hepatomegaly, portal hypertension.
Defects in JAK2 are a cause of acute myelogenous leukemia (AML) [MIM:601626]. AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development.
SEQUENCE SIMILARITIES:Belongs to the protein kinase superfamily. Tyr protein kinase family. JAK subfamily.
Contains 1 FERM domain.
Contains 1 protein kinase domain.
Contains 1 SH2 domain.
Molecular Weight
~ 125 kDa
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Evaluated by Western Blot in transfected HEK293T cell lysates.
Western Blot Analysis: 0.05 ug/mL of this antibody detected JAK-2 on 10 µg of transfected HEK293T cell lysates.
Usage Statement
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Probiotics down-regulate genes in Salmonella enterica serovar typhimurium pathogenicity islands 1 and 2. Mohamed A Bayoumi,Mansel W Griffiths Journal of food protection
73
2009
Salmonella Typhimurium pathogenesis relies mainly on the expression of genes of two pathogenicity islands, Salmonella pathogenicity islands 1 and 2 (SPI1 and SPI2). Each island has its own pattern of expression and regulation. Success in suppression of the responsible key activator of each island would be an effective way of controlling Salmonella, especially with the emerging problem of antibiotic-resistant strains. Probiotics have been shown to inhibit several foodborne pathogens, and their mode of action may partly involve down-regulation of virulence genes. To investigate whether probiotics played a role in the regulation of the pathogenicity islands SPI1 and SPI2 in Salmonella, two reporter strains were constructed in which the general regulator of SPI1, hilA, and the response regulator of SPI2, ssrB, were fused with luxCDABE genes. These constructs were used to screen the effect of probiotics on the expression of each gene. Molecules secreted by Bifidobacterium bifidum were able to down-regulate both genes.
Millipore’s JAK2 antibody demonstrates specificity against JAK2, a Janus tyrosine kinase. See below for related products for JAK2, based on the expertise of Upstate & Chemicon. Weitere Informationen >>
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