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Merck

SRP3239

Sigma-Aldrich

GDNF from rat

recombinant, expressed in E. coli, ≥98% (SDS-PAGE), ≥98% (HPLC), suitable for cell culture

Synonym(e):

ATF-1, Glial-Derived Neurotrophic Factor

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About This Item

UNSPSC-Code:
12352202
NACRES:
NA.32

Biologische Quelle

rat

Rekombinant

expressed in E. coli

Assay

≥98% (HPLC)
≥98% (SDS-PAGE)

Form

lyophilized

Mol-Gew.

15 kDa

Verpackung

pkg of 10 μg

Methode(n)

cell culture | mammalian: suitable

Verunreinigungen

<0.1 EU/μg endotoxin, tested

Farbe

white to off-white

UniProt-Hinterlegungsnummer

Versandbedingung

wet ice

Lagertemp.

−20°C

Angaben zum Gen

rat ... GDNF(25453)

Allgemeine Beschreibung

GDNF (glial cell derived neurotrophic factor) is a member of the transforming growth factor-β (TGF) superfamily. It is a potent neurotrophic factor which functions as a ligand for the multicomponent receptor complex containing GFRα1 (GDNF family receptor α1) and Ret receptor tyrosine kinase or neuronal cell adhesion molecule (NCAM). Rat GDNF is a homodimer linked by a disulfide bridge, and contains two glycosylated polypeptide chains that are released from the 211-residue-long precursor following a proteolytic cleavage.
The functional rat GDNF ligand is a disulfide-linked homodimer, of two 15.0kDa polypeptide chains called monomers. Each monomer contains seven conserved cysteine residues, one of which is used for inter-chain disulfide bridging and the others are involved in intramolecular ring formation known as the cysteine knot configuration.

Biochem./physiol. Wirkung

GDNF (glial cell derived neurotrophic factor) enhances motoneuron survival, and facilitates the survival of midbrain dopaminergic neurons which are damaged in degenerative diseases, such as Parkinson′s. In vivo and in vitro, the interaction of this protein with GDNF family receptor α1 and its co-receptor Ret tyrosine kinase, results in elevated neurite extension and survival of motor and sensory neurons. In rats with neuropathic pain, the injection of this protein in the locus coeruleus (LC) produces prolonged analgesia by increasing descending noradrenergic inhibition.

Sequenz

MSPDKQAAAL PRRERNRQAA AASPENSRGK GRRGQRGKNR GCVLTAIHLN VTDLGLGYET KEELIFRYCS GSCEAAETMY DKILKNLSRS RRLTSDKVGQ ACCRPVAFDD DLSFLDDSLV YHILRKHSAK RCGCI

Physikalische Form

Lyophilized from 10 mM Sodium Citrate.

Rekonstituierung

Centrifuge the vial prior to opening. Reconstitute in water to a concentration of 0.1-1.0 mg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 week. For extended storage, it is recommended to further dilute in a buffer containing a carrier protein (example 0.1% BSA) and store in working aliquots at -20°C to -80°C.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


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Finely Tuned Temporal and Spatial Delivery of GDNF Promotes Enhanced Nerve Regeneration in a Long Nerve Defect Model.
Marquardt LM et al
Tissue Engineering: Part A, 21(23-24), 2852-2864 (2015)
Glial cell line-derived neurotrophic factor-mediated enhancement of noradrenergic descending inhibition in the locus coeruleus exerts prolonged analgesia in neuropathic pain.
Kimura M et al
British Journal of Pharmacology, 172(10), 2469-2478 (2015)
Peripheral expression and biological activities of GDNF, a new neurotrophic factor for avian and mammalian peripheral neurons.
Trupp M et al
The Journal of Cell Biology, 130(1), 137-148 (1995)
M Trupp et al.
Nature, 381(6585), 785-789 (1996-06-27)
Glial-cell-line-derived neutrophic factor (GDNF) promotes the survival and phenotype of central dopaminergic noradrenergic and motor neurons, as well as various subpopulations of peripheral sensory and sympathetic neurons. GDNF is structurally related to members of the transforming growth factor (TGF)-beta superfamily
Weidong Xiao et al.
Molecular neurobiology, 50(2), 274-289 (2014-06-01)
Acute intestinal ischemia reperfusion (IR) injury is often associated with intestinal epithelial barrier (IEB) dysfunction. Enteric glial cells (EGCs) play an essential role in maintaining the integrity of IEB functions. However, the precise mechanism of EGCs under IR stimulation remains

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