Ambient

Triple dropout formulation (without Histidine, Leucine and Tryptophan) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Triple dropout formulation (without Histidine, Leucine and Tryptophan) with elevated Adenine of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

4 dropout formulation (without Histidine, Leucine, Tryptophan and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

4 dropout formulation (without Histidine, Leucine, Tryptophan and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Triple dropout formulation (without Histidine, Leucine and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Triple dropout formulation (without Histidine, Leucine and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Histidine and Tryptophan) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Histidine and Tryptophan) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Triple dropout formulation (without Histidine, Tryptophan and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Triple dropout formulation (without Histidine, Tryptophan and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Histidine and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Histidine and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation ( without L-Leucine) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation ( without L-Leucine) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation (without Leucine) with elevated Adenine of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Leucine and Tryptophan) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Leucine and Tryptophan) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Triple dropout formulation (without Leucine, Tryptophan and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Triple dropout formulation (without Leucine, Tryptophan and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Leucine and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Leucine and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation ( without L-Lysine) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation ( without L-Lysine) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation ( without L-Methionine) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation ( without L-Methionine) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Methionine and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Methionine and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation ( without L-Tryptophan) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation ( without L-Tryptophan) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation (without Tryptophan) with elevated Adenine of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Tryptophan and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Double dropout formulation (without Tryptophan and Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation ( without Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation ( without Uracil) of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation (without Uracil) with elevated Adenine of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

Single dropout formulation (without Uracil) with elevated Adenine of Complete Supplement Mixture (CSM) of amino acids for S. cerevisiae growth media.

CTAP, NeuroPure

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.

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.

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).

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).