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Cardiotrophin-1 Human, Mouse Monoclonal Antibody, Clone: 3G6D9

  • Regulatory status:RUO
  • Type:Monoclonal Antibody
  • Other names:CT-1, CTF1
  • Species:Human
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Cat. No. Size Price


RD182026100-01 0.1 mg
PubMed Product Details
Technical Data

Type

Monoclonal Antibody

Applications

Western blotting, Immunohistochemistry

Antibodies Applications

Source of Antigen

E. coli

Hosts

Mouse

Isotype

IgG1

Clone

3G6D9

Preparation

The antibody is a mouse monoclonal antibody against recombinant Human Cardiotrophin-1.

Amino Acid Sequence

The immunization antigen (22.5 kDa) is a protein containing 212 AA of recombinant Human Cardiotrophin-1. N-Terminal His-tag, 12 extra AA (highlighted).

MRGSHHHHHHGSSRREGSLEDPQTDSSVSLLPHLEAKIRQTHSLAHLLTKYAEQLLQEYVQLQGDPFGLPSFSPPRLPVAGLSAPAPSHAGLPVHERLRLDAAALAALPPLLDAVCRRQAELNPRAPRLLRRLEDAARQARALGAAVEALLAALGAANRGPRAEPPAATASAASATGVFPAKVLGLRVCGLYREWLSRTEGDLGQLLPGGSA

Species Reactivity

Human. Not yet tested in other species.

Purification Method

Affinity chromatography on a column with immobilized protein G.

Antibody Content

0.1 mg (determined by BCA method, BSA was used as a standard)

Formulation

The antibody is lyophilized in 0.05 M phosphate buffer, 0.1 M NaCl, pH 7.2. AZIDE FREE.

Reconstitution

Add 0.1 ml of deionized water and let the lyophilized pellet dissolve completely. Slight turbidity may occur after reconstitution, which does not affect activity of the antibody. In this case clarify the solution by centrifugation.

Shipping

At ambient temperature. Upon receipt, store the product at the temperature recommended below.

Storage/Expiration

The lyophilized antibody remains stable and fully active until the expiry date when stored at –20°C. Aliquot the product after reconstitution to avoid repeated freezing/thawing cycles and store frozen at –80°C. Reconstituted antibody can be stored at 4°C for a limited period of time; it does not show decline in activity after one week at 4°C.

Quality Control Test

Indirect ELISA – to determine titer of the antibody SDS PAGE – to determine purity of the antibody

Note

This product is for research use only.

Summary

Research topic

Cardiovascular disease

Summary

Cardiotrophin-1 (CT-1) is a 201 amino acid member of the interleukin-6 superfamily. It was identified by its ability to induce hypertrophic response in cardiac myocytes. CT-1 mRNA levels were found both in cardiac myocytes and in cardiac nonmyocytes. CT-1 was also detected in abundance in normal adult human lung and was expressed in both fetal and adult airway smooth muscle cells. CT-1activates gp130 dependent signaling and stimulates the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway to transduce hypertrophic and cytoprotective signals in cardiac myocytes. CT-1 has also a neurotrophic function. CT-1 deficiency causes increased motoneuron cell death in spinal cord and brainstem nuclei of mice during a period between embryonic day 14 and the first postnatal week. Moreover, CT-1 is a hepatocyte survival factor that efficiently reduces hepatocellular damage in animal models of acute liver injury. CT-1 expression is augmented after hypoxic stimulation and it can protect cardiac cells when added either prior to simulated ischaemia or at the time of reoxygenation following simulated ischaemia. CT-1 can induce expression of the protective heat shock proteins (hsps) in cardiac cells. Cardiotrophin-1 increased ventricular expression of ANP, brain natriuretic peptide (BNP) and angiotensinogen mRNA. CT-1 levels were significantly elevated in patients with heart failure, patients with dilatative cardiomyopathy, moderate/severe mitral regurgitation, stable and unstable angina and after acute myocardial infarction.

References to Summary

References to Cardiotrophin 1

  • Gard AL, Gavin E, Solodushko V and Pennica D: Cardiotrophin-1 in choroid plexus and the cerebrospinal fluid circulatory system. Neuroscience, 127(1):43–52 (2004)
  • Jougasaki M, Leskinen H, Larsen AM, Luchner A, Cataliotti A, Tachibana I and Burnett JC: Ventricular cardiotrophin-1 activation precedes BNP in experimental heart failure. Peptides, Jun;24(6):889–892 (2003)
  • Talwar S, Squire IB, O'brien RJ, Downie PF, Davies JE, Ng LL: Plasma cardiotrophin-1 following acute myocardial infarction: relationship with left ventricular systolic dysfunction. Clin Sci (Lond) Jan;102(1):9–14 (2002)
  • Bristow MR, Long CS: Cardiotrophin-1 in heart failure: Circulation Sep;106(12):1430–2 (2002)
  • Asai S, Saito Y, Kuwahara K, Mizuno Y, Yoshimura M, Higashikubo C, Tsuji T, Kishimoto I, Harada M, Hamanaka I, Takahashi N, Yasue H, Nakao K: The heart is a source of circulating cardiotrophin-1 in humans. Biochem Biophys Res Commun Dec;279(2):320–3 (2000)
  • Ghosh S, Ng LL, Talwar S, Squire IB, Galiñanes M: Cardiotrophin-1 protects the human myocardium from ischemic injury. Comparison with the first and second window of protection by ischemic preconditioning. Cardiovasc Res Dec;48(3):440–7 (2000)
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