144045 Results for: "peptide synthesis"

Supplier: Invitrogen

Thermo Scientific Pierce TCEP-HCl is a potent, versatile, odorless, thiol-free reducing agent with broad application to protein and other research involving reduction of disulfide bonds. The unique compound is easily soluble and very stable in many aqueous solutions. TCEP reduces disulfide bonds as effectively as dithiothreitol (DTT), but unlike DTT and other thiol-containing reducing agents, TCEP does not have to be removed before certain sulfhydryl-reactive crosslinking reactions.

Supplier: IMPLEN U.S.A. INC

Implen has become the leading expert for innovative, high-quality spectroscopy instruments and the NanoPhotometer® is trusted by thousands of researchers worldwide.

Supplier: PEPTIDES INTERNATIONAL MS

FMOC-LYS ALLOC WANG RESIN 100-200MESH 5G

Supplier: PEPTIDES INTERNATIONAL MS

CYCLO ARG-GLY-ASP-D-PHE-LYS AZIDE 5MG

Supplier: PEPTIDE SOLUTIONS, LLC MS

FMOC-BETA BETA-DIME-L-ARG(PBF)-OH 1G

Supplier: IMPLEN U.S.A. INC

Implen has become the leading expert for innovative, high-quality spectroscopy instruments and the NanoPhotometer® is trusted by thousands of researchers worldwide.

Supplier: IMPLEN U.S.A. INC

Implen has become the leading expert for innovative, high-quality spectroscopy instruments and the NanoPhotometer® is trusted by thousands of researchers worldwide.

Supplier: IMPLEN U.S.A. INC

Implen has become the leading expert for innovative, high-quality spectroscopy instruments and the NanoPhotometer® is trusted by thousands of researchers worldwide.

Supplier: IMPLEN U.S.A. INC

Implen has become the leading expert for innovative, high-quality spectroscopy instruments and the NanoPhotometer® is trusted by thousands of researchers worldwide.

Supplier: IMPLEN U.S.A. INC

Implen has become the leading expert for innovative, high-quality spectroscopy instruments and the NanoPhotometer® is trusted by thousands of researchers worldwide.

Supplier: Biosensis

GDNF is a glycosylated, disulfide-bonded homodimer molecule. It was first discovered as a potent survival factor for midbrain dopaminergic neurons and was then shown to rescue these neurons in animal models of Parkinson's disease. GDNF is about 100 times more efficient survival factor for spinal motor neurons than the neurotrophins. FUNCTION: Neurotrophic factor that enhances survival and morphological differentiation of dopaminergic neurons and increases their high-affinity dopamine uptake. SUBUNIT: Homodimer; disulfide-linked. SUBCELLULAR LOCATION: Secreted protein. ALTERNATIVE PRODUCTS: 2 named isoforms produced by alternative splicing. DISEASE: Defects in GDNF may be a cause of Hirschsprung disease (HSCR). In association with mutations of RET gene, defects in GDNF may be involved in Hirschsprung disease. This genetic disorder of neural crest development is characterized by the absence of intramural ganglion cells in the hindgut, often resulting in intestinal obstruction. DISEASE: Defects in GDNF are a cause of congenital central hypoventilation syndrome (CCHS); also known as congenital failure of autonomic control or Ondine curse. CCHS is a rare disorder characterized by abnormal control of respiration in the absence of neuromuscular or lung disease, or an identifiable brain stem lesion. A deficiency in autonomic control of respiration results in inadequate or negligible ventilatory and arousal responses to hypercapnia and hypoxemia. SIMILARITY: Belongs to the TGF-beta family. GDNF subfamily.

Supplier: Biosensis

BDNF belongs to the neurotrophin family and promotes the survival of neuronal populations that are all located either in the central nervous system or directly connected to it. It is a major regulator of synaptic transmission and plasticity at adult synapses in many regions of the CNS. The versatility of BDNF is emphasized by its contribution to a range of adaptive neuronal responses including long-term potentiation (LTP), long-term depression (LTD), certain forms of short-term synaptic plasticity, as well as homeostatic regulation of intrinsic neuronal excitability. The alterations in BDNF expression induced by various kinds of brain insult including stress, ischemia, seizure activity and hypoglycemia, may contribute to some pathologies such as depression, epilepsy, Alzheimer's, and Parkinson's disease. Microglia release BDNF that may contribute to neuroinflammation and neuropathic pain. SUBUNIT: Monomers and homodimers. Binds to NTRK2/TRKB. SUBCELLULAR LOCATION: Secreted protein. POst translation modification: Converted into mature BDNF by plasmin (PLG). SIMILARITY: Belongs to the NGF-beta family. Antibody reacts with human, mouse, rat, guinea pig BDNF. Expected to detect BDNF from other species due to sequence homology.

Supplier: Biosensis

BDNF belongs to the neurotrophin family and promotes the survival of neuronal populations that are all located either in the central nervous system or directly connected to it. It is a major regulator of synaptic transmission and plasticity at adult synapses in many regions of the CNS. The versatility of BDNF is emphasized by its contribution to a range of adaptive neuronal responses including long-term potentiation (LTP), long-term depression (LTD), certain forms of short-term synaptic plasticity, as well as homeostatic regulation of intrinsic neuronal excitability. The alterations in BDNF expression induced by various kinds of brain insult including stress, ischemia, seizure activity and hypoglycemia, may contribute to some pathologies such as depression, epilepsy, Alzheimer's, and Parkinson's disease. Microglia release BDNF that may contribute to neuroinflammation and neuropathic pain. SUBUNIT: Monomers and homodimers. Binds to NTRK2/TRKB. SUBCELLULAR LOCATION: Secreted protein. POst translation modification: Converted into mature BDNF by plasmin (PLG). SIMILARITY: Belongs to the NGF-beta family. Antibody reacts with human, mouse, rat, guinea pig BDNF. Expected to detect BDNF from other species due to sequence homology.

Supplier: Genetex

Jun activation domain-binding protein 1 (JAB1) also designated COP9 subunit 5 (COPS5) or SGN5 is a coactivator of AP1 transcription factor that also promotes degradation of the cyclin-dependent kinase inhibitor p27Kip1. JAB1 interacts with c-Jun AP1 containing complexes, and enhances transactivation from AP1 dependent promoters. It also interacts with Jun D but not with Jun B or v-Jun. JAB1 is highly conserved in evolution and is widely expressed in mammalian tissues. It is localized both the nucleus and the cytoplasm. It interacts with the cytoplasmic domain of the alphaL/beta2 integrin LFA1. Following LFA1 engagement the nuclear pool of JAB1 increases and activation of an AP1 driven promoter is enhanced. Interaction of JAB1 with the nuclear progesterone receptor and the steroid receptor activator (SRC1) was reported. JAB1 is a stability and activity regulator of Hypoxia - inducible factor 1 (HIF1), a transcription factor that controls activation of several genes responsive to the cellular oxygen tension. The macrophage migration inhibitory factor (MIF) associates with JAB1 in the cytosol near the plasma membrane. Endogenous MIF inhibits JAB1-induced AP1 transcriptional activity. JAB1 is a subunit of the COP9 regulatory complex. COP9 cleaves the ubiquitin-like protein Nedd8 from the Cul1 subunit of SCF ubiquitin ligases. A metalloprotease motif in JAB1 plays a role in this isopeptidase activity. Breakdown of the cyclin dependent kinase inhibitor p27Kip1 is promoted by JAB1. The latter expression in several cancers inversely correlates with p27Kip1 and may reflect tumor aggressiveness. A possible involvement of JAB1 in atherosclerosis was also reported. Involvement of JAB1 in degradation of the suppressors p53 and smad4 was described recently.

Supplier: Bachem Americas

Sequence: H-Cys-OH · HCl · H₂O