1mg

Molecular Formula : C17H16O5

Ciliary Neurotrophic Factor (CNTF) is a cytokine belonging to the Interleukin 6 (IL-6) family, which also includes IL-6, Oncostatin M, Leukemia Inhibitory Factor (LIF), and Cardiotrophin-1. Structurally, CNTF resembles a four-helix bundle composition, similar to the other members of the IL-6 family. The receptor for CNTF is composed of three parts: a gp130-like subunit common in the IL-6 receptor family, a LIF Receptor β subunit, and a CNTF specific α receptor subunit. Upon binding to the CNTF, the β subunit of the CNTF receptor will undergo tyrosine phosphorylation, and activate the intracellular JAK/STAT pathway. The main function of CNTF in vivo is to promote the differentiation and survival of a variety of neurons and glial cells, including sympathetic precursor cells and spinal motor neurons.

Ciliary neurotrophic factor (CNTF) is a polypeptide hormone whose actions appear to be restricted to the nervous system where it promotes neurotransmitter synthesis and neurite outgrowth in certain neuronal populations. CNTF was initially identified as a trophic factor for embryonic chick ciliary parasympathetic neurons in culture. Furthermore, the protein is also a potent survival factor for neurons and oligodendrocytes and may be relevant in reducing tissue destruction during inflammatory attacks. In addition, CNTF is useful for treatment of motor neuron disease and it could reduce food intake without causing hunger or stress. Recombinant murine CNTF containing 198 amino acids and it shares 82 % and 95 % a.a. sequence identity with human and rat CNTF.

Ciliary Neurotrophic Factor (CNTF) is a polypeptide hormone which acts within the nervous system where it promotes neurotransmitter synthesis and neurite outgrowth in certain neuronal populations. CNTF is a potent survival factor for neurons and oligodendrocytes and may play a role in reducing tissue damage during increased inflammation. A mutation in this gene, which results in aberrant splicing, leads to ciliary neurotrophic factor deficiency, however this phenotype is not causally related to neurologic disease.

Molecular Formula : C17 2H3 H18 N O4

Molecular Formula : C24H28NNaO9

Molecular Formula : C24H23D6NO9

Molecular Formula : C18 2H3 H18 N O3

Molecular Formula : C24 2H3 H25 N O9 . Na

Molecular Formula : C18 2H6 H15 N O3

Molecular Formula : C26 H21 N3 O2

Molecular Formula : C44H72N7O17P3S • x(Na)

Molecular Formula : C26 H35 N9 Na3 O17 P3 S

Molecular Formula : C54 H82 O4

Molecular Formula : C22 2H3 H22 N O6

Molecular Formula : C22 H19 D6 N O6

Molecular Formula : C12 D9 H10 N O3 . H Cl

Molecular Formula : C20H22O6

Molecular Formula : C27H24F2N4O3

Molecular Formula : C29 H42 O10

Molecular Formula : C10 H15 N3 O8

Molecular Formula : C40H46N4O8

Molecular Formula : C36H3815N4O8

Molecular Formula : C36 H38 N4 O8 . 2Cl 2H

Molecular Formula : C27 H22 O18

Molecular Formula : C24 2H12

Molecular Formula : C208H344N60O63S2 • x(C2HF3O2)

Molecular Formula : C27 H37 O11 . Na

Molecular Formula : C21 2H4 H26 O5

Molecular Formula : C21 D3 H27 O5

Molecular Formula : C21 D8 H20 O5

Molecular Formula : C16 H18 N2 O6

Molecular Formula : C16H20N2O7

Molecular Formula : C16 H20 N2 O7

Molecular Formula : C19 D4 H11 Cl O4

Molecular Formula : C14 2H10 H6 Cl O5 P S

Molecular Formula : C19 D4 H12 O3

Molecular Formula : C13C3H9N3O2

Molecular Formula : C4 2H3 H4 N3 O

Molecular Formula : C23H9D5Na2O11

Molecular Formula : C7H5D9ClNO2

C-reactive protein (CRP) is synthesized in the liver by macrophage. Its level in blood increases when inflammation occurs. CRP serves as a useful marker for diagnosis of inflammation. High-sensitivity C-reactive protein (hsCRP), can serve as a risk marker for the diagnosis of myocardial infarction, ischemic stroke, peripheral vascular disease. Measuring hsCRP in blood is helpful to provide positive treatment of the disease.

C-reactive protein (CRP) is synthesized in the liver by macrophage. Its level in blood increases when inflammation occurs. CRP serves as a useful marker for diagnosis of inflammation. High-sensitivity C-reactive protein (hsCRP), can serve as a risk marker for the diagnosis of myocardial infarction, ischemic stroke, peripheral vascular disease. Measuring hsCRP in blood is helpful to provide positive treatment of the disease.

Cytotoxic T lymphocyte-associated molecule-4 (CTLA-4) is a cell surface molecule that is closely related to CD28, and a powerful negative regulator of T cell activation. Structurally, CTLA-4 is a member of the Ig superfamily, having a single extracellular V-like domain , homology with CD28; The overall sequence homology between CD28 and CTLA-4 is about 20%, but they share a 27% (murine) to 31% (human) identity at the amino acid level. Inhibitory receptor acting as a major negative regulator of T-cell responses. The affinity of CTLA-4 for its natural B7 family ligands, CD80 and CD86, is considerably stronger than the affinity of their cognate stimulatory coreceptor CD28.

CTLA-4 (Cytotoxic T-Lymphocyte Antigen 4) is also known as CD152, is an Inhibitory receptor acting as a major negative regulator of T-cell responses. CTLA-4 is a member of the immunoglobulin superfamily, which is expressed on the surface of T cells and transmits an inhibitory signal to T cells. CTLA-4 and CD28 are homologous receptors expressed by both CD4+ and CD8+ T cells, which mediate opposing functions in T-cell activation. Both receptors share a pair of ligands expressed on the surface of antigen-presenting cells (APCs). The affinity of CTLA-4 for its natural B7 family ligands, CD80 and CD86, is considerably stronger than the affinity of their cognate stimulatory co-receptor CD28.

Cardiac Troponin I (cTnI) is synthesized in cardiac muscle and forms a structural complex with Troponin T and C. Its concentration in blood increases after the onset of chest pain and maintains peak for a couple of weeks. The cTnI protein is considered as useful diagnosis marker for acute myocardial infarction (AMI).

Cardiac Troponin I (cTnI) is synthesized in cardiac muscle and forms a structural complex with Troponin T and C. Its concentration in blood increases after the onset of chest pain and maintains peak for a couple of weeks. The cTnI protein is considered as useful diagnosis marker for acute myocardial infarction (AMI).

Cardiac Troponin I (cTnI) is synthesized in cardiac muscle and forms a structural complex with Troponin T and C. Its concentration in blood increases after the onset of chest pain and maintains peak for a couple of weeks. The cTnI protein is considered as useful diagnosis marker for acute myocardial infarction (AMI).

Cardiac Troponin I (cTnI) is synthesized in cardiac muscle and forms a structural complex with Troponin T and C. Its concentration in blood increases after the onset of chest pain and maintains peak for a couple of weeks. The cTnI protein is considered as useful diagnosis marker for acute myocardial infarction (AMI).

Cardiac Troponin I (cTnI) is synthesized in cardiac muscle and forms a structural complex with Troponin T and C. Its concentration in blood increases after the onset of chest pain and maintains peak for a couple of weeks. The cTnI protein is considered as useful diagnosis marker for acute myocardial infarction (AMI).