Cardiotrophin-1 Human (E. coli)

Description

Total 212 AA. MW: 22.5 kDa (calculated). N-Terminal His-tag, 12 extra AA (highlighted).

Amino Acid Sequence

Source

E. coli

Purity

>90%

SDS-PAGE gel

12% SDS-PAGE separation of Human Cardiotrophin 1. M.W. marker – 14, 21, 31, 45, 66, 97 kDa 2. reduced and heated sample, 10μg/lane 3. non-reduced and non-heated sample, 10μg/lane

Formulation

Filtered (0,4 μm) and lyophilized in 0.5 mg/mL in 0.05M Acetate buffer pH4.

Reconstitution

Add 0.1M Acetate buffer pH4 to prepare a working stock solution of approximately 0.5 mg/mL and let the lyophilized pellet dissolve completely. For conversion into higher pH value, we recommend intensive dilution by relevant buffer to a concentration of 10μg/mL. In higher concentrations the solubility of this antigen is limited. Product is not sterile! Please filter the product by an appropriate sterile filter before using it in the cell culture.

Storage, Stability/Shelf Life

Store lyophilized protein at –20°C. Lyophilized protein remains stable until the expiry date when stored at –20°C. Aliquot reconstituted protein to avoid repeated freezing/thawing cycles and store at –80°C for long term storage. Reconstituted protein can be stored at 4°C for a limited period of time; it does not show any change after two weeks at 4°C.

Quality Control Test

BCA to determine quantity of the protein.

SDS PAGE to determine purity of the protein.

Applications

ELISA, Western blotting

Note

This product is intended for research use only.

Introduction to the Molecule

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

• Liao Z, Brar BK, Cai Q, Stephanou A, O'Leary RM, Pennica D, Yellon DM, Latchman DS. Cardiotrophin-1 (CT-1) can protect the adult heart from injury when added both prior to ischaemia and at reperfusion. Cardiovasc Res. 2002 Mar; 53(4): 902-10.
• Bristow MR, Long CS. Cardiotrophin-1 in heart failure. Circulation. 2002 Sep 17; 106(12): 1430-2.
• Freed DH, Moon MC, Borowiec AM, Jones SC, Zahradka P, Dixon IM. Cardiotrophin-1: expression in experimental myocardial infarction and potential role in post-MI wound healing. Mol Cell Biochem. 2003 Dec; 254(1-2): 247-56.
• Freed DH, Borowiec AM, Angelovska T, Dixon IM. Induction of protein synthesis in cardiac fibroblasts by cardiotrophin-1: integration of multiple signaling pathways. Cardiovasc Res. 2003 Nov 1; 60(2): 365-75.
• 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). 2002 Jan; 102(1): 9-14.