Anti-Ras (K-,H-,N-), clone 9A11.2 (mouse monoclonal)

Species Reactivity	Key Applications	Host	Format	Antibody Type
H, M, R	WB, IH(P)	M	Purified	Monoclonal Antibody

Species Reactivity

Key Applications

Host

Format

Antibody Type

H, M, R

WB, IH(P)

Purified

Monoclonal Antibody

Description
Catalogue Number	05-1072
Brand Family	Upstate
Trade Name	Upstate
Description	Anti-Ras Antibody, (K-, H-, N-), clone 9A11.2
Background Information	Ras, a proto-oncogene, is a small G-protein that has 3 primary isoforms (H-Ras, N-Ras, and K-Ras) that differ in there approximately 20 C-terminal amino acids. H-Ras was first discovered as a transforming product the retrovirus Harvey murine virus and K-Ras of Kirten sarcoma virus. Ras is a heavily studied target of both academic and pharmaceutical research because of its implications in various pathways and diseases as well as being mutated in a large number of human cancers. Ras is most notably the activator of the Erk/MAPK kinase pathway as activator of Raf, as well as an activator of PI3 Kinase (PI3K). 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. For this to take place, a controlled three step process must occur. The first step in the process is the prenylation or geranylation of the C in the CAAX motif that is initiated by the covalent attachment of farnesyl groups to the cysteine that is catalyzed by the heterodimer enzymes farnesyl transferases and . After this modification, the –aaX of the motif is proteolytically removed via Rce1 (Ras Converting Enzyme 1), a membrane associated endoprotease, by a mechanism that is still not fully understood. Finally, the C-terminal prenylcysteine is now methlylated by ICMT (Isoprenylcysteine Carboxymethyl Transferase). 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.

Description

Catalogue Number

05-1072

Brand Family

Upstate

Trade Name

Upstate

Description

Anti-Ras Antibody, (K-, H-, N-), clone 9A11.2

Background Information

Ras, a proto-oncogene, is a small G-protein that has 3 primary isoforms (H-Ras, N-Ras, and K-Ras) that differ in there approximately 20 C-terminal amino acids. H-Ras was first discovered as a transforming product the retrovirus Harvey murine virus and K-Ras of Kirten sarcoma virus. Ras is a heavily studied target of both academic and pharmaceutical research because of its implications in various pathways and diseases as well as being mutated in a large number of human cancers. Ras is most notably the activator of the Erk/MAPK kinase pathway as activator of Raf, as well as an activator of PI3 Kinase (PI3K). 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. For this to take place, a controlled three step process must occur. The first step in the process is the prenylation or geranylation of the C in the CAAX motif that is initiated by the covalent attachment of farnesyl groups to the cysteine that is catalyzed by the heterodimer enzymes farnesyl transferases and . After this modification, the –aaX of the motif is proteolytically removed via Rce1 (Ras Converting Enzyme 1), a membrane associated endoprotease, by a mechanism that is still not fully understood. Finally, the C-terminal prenylcysteine is now methlylated by ICMT (Isoprenylcysteine Carboxymethyl Transferase). 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.

Product Information
Format	Purified
Presentation	Protein G purified mouse monoclonal in storage buffer containing 0.1M Tris-Glycine (pH 7.4), 15mM NaCl, and 0.05% NaN3.

Product Information

Format

Purified

Presentation

Protein G purified mouse monoclonal in storage buffer containing 0.1M Tris-Glycine (pH 7.4), 15mM NaCl, and 0.05% NaN3.

Applications
Application	This Anti-Ras Antibody, (K-, H-, N-), clone 9A11.2 is validated for use in WB, IH(P) for the detection of Ras.
Key Applications	Western Blotting Immunohistochemistry (Paraffin)

Applications

Application

This Anti-Ras Antibody, (K-, H-, N-), clone 9A11.2 is validated for use in WB, IH(P) for the detection of Ras.

Key Applications

Western Blotting
Immunohistochemistry (Paraffin)

Biological Information
Immunogen	Full length recombinant GST-tagged human H-Ras.
Clone	9A11.2
Concentration	Please refer to the Certificate of Analysis for the lot-specific concentration.
Host	Mouse
Specificity	Recognizes K-, H-, and N-Ras (all 3 isofroms).
Isotype	IgG1κ
Species Reactivity	Human Mouse Rat
Antibody Type	Monoclonal Antibody
Entrez Gene Number	NM_005343
Entrez Gene Summary	Members of the RAS superfamily of GTP-binding proteins, which includes MRAS, are membrane-anchored, intracellular signal transducers responsible for a variety of normal cellular functions. They are oncogenically activated in a significant fraction of tumors.[supplied by OMIM]
Gene Symbol	K-Ras Ki-Ras K-Ras2 Kras-2 p21B KRAS RASK2 HRAS HA_RAS N-RAS H-RAS NRAS NRAS1 ALPS4
Purification Method	Protein G Purified
UniProt Number	P01116
UniProt Summary	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). SIZE: 189 amino acids; 21,656 Da SUBUNIT: Interacts with PHLPP (By similarity). 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. Defects 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. Defects 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.
Molecular Weight	21 kDa

Biological Information

Immunogen

Full length recombinant GST-tagged human H-Ras.

Clone

9A11.2

Concentration

Please refer to the Certificate of Analysis for the lot-specific concentration.

Host

Mouse

Specificity

Recognizes K-, H-, and N-Ras (all 3 isofroms).

Isotype

IgG1κ

Species Reactivity

Human
Mouse
Rat

Antibody Type

Monoclonal Antibody

Entrez Gene Number

NM_005343

Entrez Gene Summary

Members of the RAS superfamily of GTP-binding proteins, which includes MRAS, are membrane-anchored, intracellular signal transducers responsible for a variety of normal cellular functions. They are oncogenically activated in a significant fraction of tumors.[supplied by OMIM]

Gene Symbol

K-Ras
Ki-Ras
K-Ras2
Kras-2
p21B
KRAS
RASK2
HRAS
HA_RAS
N-RAS
H-RAS
NRAS
NRAS1
ALPS4

Purification Method

Protein G Purified

UniProt Number

P01116

UniProt Summary

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).
SIZE: 189 amino acids; 21,656 Da
SUBUNIT: Interacts with PHLPP (By similarity).
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.

Defects 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.

Defects 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.

Molecular Weight

21 kDa

Product Usage Statements
Quality Assurance	routinely evaluated by immunoblot on RIPA lysate from human A431 carcinoma cells, mouse 3T3, mouse brain, orrat brain.
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.

Product Usage Statements

Quality Assurance

routinely evaluated by immunoblot on RIPA lysate from human A431 carcinoma cells, mouse 3T3, mouse brain, orrat brain.

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.

Storage and Shipping Information
Storage Conditions	Stable for 1 year at 4°C from date of receipt. Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution.

Storage and Shipping Information

Storage Conditions

Stable for 1 year at 4°C from date of receipt.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution.

Packaging Information
Material Size	100 µg

Packaging Information

Material Size

100 µg

实验耗材

分子生物学试剂

蛋白与免疫学

生化试剂

细胞及检测试剂

色谱及层析

仪器设备

实验服务

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Anti-Ras (K-,H-,N-), clone 9A11.2 (mouse monoclonal)

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