anti-Cardiotrophin 1 (CTF1) Antikörper

Human Cardiotrophin 1 (CTF1) Interaktionspartner

1. a transcriptional factor, Myc-associated zinc finger protein (MAZ (zeige MAZ Antikörper)), plays an important role in ADAM10 (zeige ADAM10 Antikörper) transcription in response to CT-1 in neural stem/progenitor cells.

2. CT-1 was found to be associated with Tn-I, which is used to detect myocardial damage after OPCAB surgery. CT-1 may also be used to detect myocardial damage.

3. non-diabetic subjects who were overweight or obesity had significantly lower cardiotrophin-1 concentrations than those with normal weight, and both obesity and being overweight were inversely associated with cardiotrophin-1 levels.

4. This paper will review many aspects of CT-1 physiological role in several organs and discuss data for consideration in therapeutic approaches.

5. biliary epithelium-derived CT-1 may exert a profibrogenic potential in PCLD (zeige PRKCSH Antikörper).

6. Data show that cardiotrophin-1 is positively related to brachial-ankle pulse-wave velocity (baPWV) independent of traditional cardiometabolic risk factors for arterial stiffness.

7. this study, even though preliminary and awaiting further confirmation by independent replication, provides first evidence that common genetic variation in CTF1 could contribute to insulin (zeige INS Antikörper) sensitivity in humans.

8. Study correlates CT-1 levels with ambulatory and central BP, as well as with pulse wave velocity in patients with essential hypertension.

9. CT-1 is differentially induced in the myocardium of infants with congenital cardiac defects depending on hypoxemia, and may mediate myocardial hypertrophy and dysfunction.

10. Subjects with impaired glucose tolerance (IGT) and newly diagnosed diabetes (NDD) have significantly higher CT-1 concentrations than those with normal glucose tolerance. IGT and NDD are positively associated with CT-1 concentrations.

Mouse (Murine) Cardiotrophin 1 (CTF1) Interaktionspartner

1. These results suggest that CT-1 may be a potent candidate for the early prevention and treatment of Alzheimer disease.

2. Identify cardiotrophin-1 as a powerful cytokine promoting mesenchymal stromal cell engraftment and thus improving cell therapy of the infarcted myocardium.

3. CT-1 mRNA levels in adipose tissue showed significant circadian fluctuations in young WT mice. Clock genes displayed a circadian rhythm in adipose tissue of both wild-type (WT) and CT-1-/- mice. However, the pattern was altered in CT-1-/- mice toward a lower percentage of the rhythm or lower amplitude, especially for Bmal1 (zeige ARNTL Antikörper) and Clock.

4. Cardiotrophin-1 modulates the production of adipokines in vitro and in vivo, suggesting that the regulation of the secretory function of adipocytes could be involved in the metabolic actions of this cytokine.

5. Nuclear translocation of CT-1 regulates cardiomyogenesis of ES cells and involves calcium, NO, ROS (zeige ROS1 Antikörper) as well as CT-1 regulated signaling pathways.

6. Data suggest that Ctf1 up-regulates lipolysis in white adipocytes via 1) induction of perilipin (zeige PLIN1 Antikörper), 2) activation of hormone sensitive lipase (zeige LIPE Antikörper) (via phosphorylation by PKA), and 3) inactivation of adipose triglyceride lipase (zeige PNPLA2 Antikörper) (via up-regulation of G0S2 (zeige G0S2 Antikörper)).

7. Cardiotrophin-1 (CT-1) is a hepatoprotective cytokine that modulates fat and glucose metabolism. Here we analyzed the changes in hepatic fat stores induced by recombinant CT-1 and its therapeutic potential in non-alcoholic fatty liver disease.

8. The transgenic expression of CTF1 brought about a marked improvement on cognitive functioning in the APPswe/PS1dE9 transgenic mouse model of Alzheimer's disease.

9. CT-1 improves beta cell function and survival, and protects mice against STZ-induced diabetes

10. CT-1 may be a major regulator of arterial stiffness with a major impact on the aging process.

Pig (Porcine) Cardiotrophin 1 (CTF1) Interaktionspartner

1. CT1 (zeige SLC6A8 Antikörper) decreases cell death through a mechanism related to Stat3 (zeige STAT3 Antikörper) and Akt (zeige AKT1 Antikörper) phosphorylation and activation of calpastatin (zeige CAST Antikörper) in D-galactosamine-treated hepatocytes.