货号:15-108
品牌:Merck Millipore
规格:EA
目录价:询价
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Description:
MAPK Pathway 2 Explorer Antibody MiniPack
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Promotional Text:
Special Shipping Offer on Antibodies100% Performance Guaranteed
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Trade Name:
Upstate (Millipore)
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Specificity:
05-1072SP: Recognizes K-Ras, H-Ras, and N-Ras.;05-797RSP:Recognizes Erk 1 & 2 only when dually phosphorylated on its TxY activation motif.;05-538SP:Recognizes Raf-1 phosphorylated at Serine 338
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Molecular Weight:
05-1072SP: 21 kDa; 05-797RSP: 42 & 44 kDa; 05-538SP: 74 kDa
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Modifications:
Phosphorylation
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Clone:
05-1072SP: 9A11.2; 05-797RSP: AW39R
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Background Information:
Pathway Explorer Antibody MiniPack:Each Pathway Explorer Antibody Minipack contains three related antibodies as part of a signaling cascade or a combination of total and phosphorylated forms of key signaling targets. Each of the three antibodies are 30% the original pack size. Full size versions of each of the Pathway Explorer antibodies are available for sale individually under the same catalog number with the removal of “SP” off of each one (e.g. 05-591SP can be ordered as 05-591). Ras:Ras, a proto-oncogene, is a small G-protein that has 3 primary isoforms (H-Ras, N-Ras, and K-Ras). They differ in their approximately 20 C-terminal amino acids. In its oncogenic, mutated state, Ras is unable to hydrolyze GTP to GDP, thus staying in an active state and activating numerous pathways including the MAPK pathway through its activation of Raf, but also others as well that include PI3 Kinase and RalGDS. One path that the pharmaceutical industry has taken to control Ras and its activity is by finding what some consider its Achilles’ heel. For its activation, Ras must localize to the plasma membrane, but interestingly, it lacks a transmembrane domain. To achieve this, Ras must first undergo a post-translational modification (PTM) known as prenylation or geranylation at its C-terminal CAAX motif. These drugs have yet to pass clinical trials though and there is doubt that they will ever be successful in treating tumors associated with Ras activation.Raf: The Raf proteins (A-Raf, B-Raf, Raf-1/c-Raf) are Ser/Thr kinases with homology to the PKC family, containing an N-terminal regulatory domain and a C-terminal catalytic domain. Raf (MAP Kinase Kinase Kinase) is the top kinase in the canonical MAPK pathway. Members of the Raf family bind to activated Ras. Ras, in its GTP-bound active state, activates the kinase activity of Raf. This results in Raf translocation to the plasma membrane and activation. Once activated, Raf then binds to and activates MEK (MAP Kinase Kinase) by phosphorylating it on the two residue motif. It is thought that B-Raf might be the predominant activator of MEK and that Raf-1 has a role in protection against apoptosis; a process that does not require either its kinase activity or its activation of MEK. The regulation of a large number of cellular processes are dependent upon the activation state of ERK, so the controlling of this pathway could have profound effects on various diseases. Activation of Raf-1 involves phosphorylation of Ser338/339 and Tyr340/341. Activating mutations of B-Raf that disrupt its auto-inhibition loop have been implicated in a number of cancers, including melanoma and colon cancer.Erk:Erk (Extracellular signal-Related Kinase) is a family of two, highly homologous proteins denoted as Erk1 (p44, MAPK3) and Erk2 (p42, MAPK1) that both function in the same pathway. The two proteins are often referred to collectively as Erk1/2 or p44/p42 MAP kinase. The Erk pathway is considered the classical, canonical MAPK (Mitogen-Activated Protein Kinase) signaling pathway. It is an evolutionarily conserved pathway that controls and is a critical regulator of the growth and survival through the promotion of cell proliferation and the prevention of apoptosis. Erk is involved in the control of many fundamental cellular processes including cell proliferation, survival, differentiation, apoptosis, motility and metabolism. Erk is activated by growth factor stimulation of receptor tyrosine kinases (RTKs), GPCR, and/or integrin stimulation. This activates the Ras-Raf-MEK-Erk pathway that results in the phosphorylation/activation of Erk1/2 (p44/p42) on the TxY motif (Thr202/Tyr204 and Thr185/Tyr187 for Erk1 & Erk2, respectively). * See full size versions for corresponding references.
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Species Reactivity:
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Human
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Mouse
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Rat
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E. coli
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Chicken
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Xenopus
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Species Reactivity Note:
05-538SP:Mouse and human.Predicted to cross react with rat, chicken and Xenopus based on sequence homology.
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Application Notes:
05-1072SP: Immunohistochemistry: Antibody was diluted to 1:50, IHC Select Detection System HRP/DAM.; 05-797RSP: Immunofluorescence Analysis: A431 cells were fixed, permabilized and dual stained with anti-phospho-Erk 1/2 ; Flow Cytometry Analysis:Jurkat cells were fixed, permeablized, and stained with anti-phospho-Erk 1/2 (Thr202/Tyr204, Thr185/Tyr187), recombinant clone AW39 at a 1:100 dilution.;
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Control:
For 05-538SP use 3T3/NIH cells
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Presentation:
3 individual tubes containing either Anti-phospho-Erk 1/2(Thr202/Tyr204, Thr185/Tyr187), recombinant clone AW39R ; Anti-phospho-Raf-1 (Ser338); Anti-Ras (K-,H-,N-), clone 9A11.2
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Storage Conditions:
05-1072SP: Stable for 1 year at 2-8°C from date of receipt.Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution.; 05-797RSP and 05-538SP:Stable for 1 year at -20°C from date of receipt.Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.
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UniProt Number:
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P01116
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P01112
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P04049
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P27361
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P28482
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Entrez Gene Number:
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NP_203524
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NP_002871
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NP_203524
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NP_005334
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NP_002737
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NP_002736
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Gene Symbol:
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Erk1
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Erk2
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p44-MAPK
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p42-MAPK
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MAPK2
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PRKM2
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p41mapk
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PRKM1
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p44
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ERK2
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P42MAPK
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ERK
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p42
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MAPK1
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ERT1
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ERT2
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Mitogen-activated protein kinase
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MAP Kinase 2
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MAP Kianse 1
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MAPK
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C-RAF
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CRAF
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EC 2.7.11.1
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NS5
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RAF
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Raf-1
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Alternate Names:
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Oncogene RAF1
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raf proto-oncogene serine/threonine protein kinase
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mitogen activated protein kinase
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MAP Kinase 2
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MAP Kinase 1
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Ras
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KRAS
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GTPase Ras
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Components:
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05-797RSP Anti-phospho-Erk 1/2(Thr202/Tyr204, Thr185/Tyr187), recombinant clone AW39R
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05-538SP Anti-phospho-Raf-1 (Ser338)
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05-1072SP Anti-Ras (K-,H-,N-), clone 9A11.2
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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.
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Key Applications:
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Western Blotting
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Flow Cytometry
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Immunofluorescence
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Immunohistochemistry
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Multiplexing
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UniProt Summary:
K-Ras:FUNCTION: Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.ENZYME REGULATION: Alternate between an inactive form bound to GDP and an active form bound to GTP. Activated by a guanine nucleotide-exchange factor (GEF) and inactivated by a GTPase-activating protein (GAP).SUBUNIT STRUCTURE: Interacts with PHLPP SUBCELLULAR LOCATION: Cell membrane; Lipid-anchor; Cytoplasmic side. INVOLVEMENT IN DISEASE:Defects in KRAS 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. Ref.20Defects in KRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:607785]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. It is characterized by leukocytosis with tissue infiltration and in vitro hypersensitivity of myeloid progenitors to granulocyte-macrophage colony stimulating factor.Defects in KRAS are the cause of Noonan syndrome 3 (NS3) [MIM:609942]. Noonan syndrome (NS) [MIM:163950] is a disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis. It is a genetically heterogeneous and relatively common syndrome, with an estimated incidence of 1 in 1000-2500 live births. Rarely, NS is associated with juvenile myelomonocytic leukemia (JMML). NS3 inheritance is autosomal dominant. Ref.23Defects in KRAS are a cause of cardiofaciocutaneous syndrome (CFC syndrome) [MIM:115150]; also known as cardio-facio-cutaneous syndrome. CFC syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. Heart defects include pulmonic stenosis, atrial septal defects and hypertrophic cardiomyopathy. Some affected individuals present with ectodermal abnormalities such as sparse, friable hair, hyperkeratotic skin lesions and a generalized ichthyosis-like condition. Typical facial features are similar to Noonan syndrome. They include high forehead with bitemporal constriction, hypoplastic supraorbital ridges, downslanting palpebral fissures, a depressed nasal bridge, and posteriorly angulated ears with prominent helices. The inheritance of CFC syndrome is autosomal dominant.KRAS mutations are involved in cancer development.Raf-1:FUNCTION: Involved in the transduction of mitogenic signals from the cell membrane to the nucleus. Part of the Ras-dependent signaling pathway from receptors to the nucleus. Protects cells from apoptosis mediated by STK3.CATALYTIC ACTIVITY: ATP + a protein = ADP + a phosphoprotein.COFACTOR: Binds 2 zinc ions per subunit.SUBUNIT STRUCTURE: Interacts with Ras proteins. The interaction with Ras is antagonized by RIN1. Weakly interacts with RIT1 By similarity. Interacts with STK3, which inhibits its pro-apoptotic activity. TISSUE SPECIFICITY: In skeletal muscle, isoform 1 is more abundant than isoform 2.POST-TRANSLATIONAL MODIFICATION: Phosphorylated upon DNA damage, probably by ATM or ATR. Phosphorylation at Thr-269 increases its kinase activity. INVOLVEMENT IN DISEASE: Defects in RAF1 are the cause of Noonan syndrome type 5 (NS5) [MIM:611553]. Noonan syndrome (NS) is a disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis. It is a genetically heterogeneous and relatively common syndrome, with an estimated incidence of 1 in 1000-2500 live births. Ref.24 Ref.25Defects in RAF1 are the cause of LEOPARD syndrome type 2 (LEOPARD syndrome-2) [MIM:611554]. LEOPARD syndrome is an autosomal dominant disorder allelic with Noonan syndrome. The acronym LEOPARD stands for lentigines, electrocardiographic conduction abnormalities, ocular hypertelorism, pulmonic stenosis, abnormalities of genitalia, retardation of growth, and deafness.Erk2:FUNCTION: Catalyzes the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in MAP kinases. Activates ERK1 and ERK2 MAP kinases. CATALYTIC ACTIVITY: ATP + a protein = ADP + a phosphoprotein.ENZYME REGULATION: Activated by phosphorylation on tyrosine and threonine in response to insulin and NGF. Both phosphorylations are required for activitySUBUNIT STRUCTURE: Interacts with MORG1 By similarity. Binds to HIV-1 Nef through its SH3 domain. This interaction inhibits its tyrosine-kinase activity. Interacts with its substrates HSF4 and ARHGEF2. Interacts with NISCH.DOMAIN: The TXY motif contains the threonine and tyrosine residues whose phosphorylation activates the MAP kinases.PTM: Dually phosphorylated on Thr-185 and Tyr-187, which activates the enzyme.
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Brand Family:
Upstate
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Product Name:
MAPK Pathway 2 Explorer Antibody MiniPack
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Concentration:
05-1072SP and 05-538SP: 1 mg/mL
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Antibody Type:
Monoclonal Antibody
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Qty/Pk:
3 vials/Pk
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Format:
Purified
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Properties:
Each vial is 30% the size of the parent catalog number
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