mog

Myelin Oligodendrocyte Glycoprotein Peptide (35-55), mouse, rat (MOG (35-55)), is a truncated peptide derived from the human Myelin Oligodendrocyte Glycoprotein (MOG).

Myelin Oligodendrocyte Glycoprotein (MOG) peptide (35-55) , mouse, rat acetate is a MOG peptide (35-55) derivative. MOG peptide (35-55) is a part of myelin oligodendrocyte glycoprotein (MOG) immunogenic peptide and can be used to study immune-related diseases.

Myelin oligodendrocyte glycoprotein (MOG) peptide, a truncated form of MOG located on the extracellular myelin sheath surface, interacts with antigen serotype HLA-DR2 to mitigate effects of ischemic stroke induced by middle cerebral artery occlusion (MCAO) in mice. In female mice, it notably reduces cortical and striatal infarct volumes, lessens sensorimotor deficits as observed in tube- and corner turn tests, enhances engagement with novel odors, and prolongs the duration of cage mate-directed vocalizations, without exhibiting similar outcomes in male mice.

Myelin Oligodendrocyte Glycoprotein Peptide (35-55), mouse, rat (TFA) is a minor component of CNS myelin.

MOG (35-55), human, a constituent of central nervous system myelin, is distinguishable from mMOG (35-55) due to a proline-to-serine substitution at position 42. It possesses immunogenic properties and is partially cross-reactive with mMOG35–55. However, MOG (35-55), human does not induce encephalitogenic effects, and only elicits minimal clinical signs of EAE (experimental autoimmune encephalomyelitis) in comparison to the rodent peptide.

MOG (89-113), human is a peptide fragment of human myelin oligodendrocyte glycoprotein.

MOG peptide (35-55), a myelin oligodendrocyte glycoprotein (MOG) fragment spanning amino acids 35 to 55, selectively stimulates CD4+ T cell expansion and induces experimental autoimmune encephalomyelitis (EAE) in animal models [1] [2] [3].

MOG (92–106), mouse, rat, is a biologically active peptide corresponding to the fragment of amino acids 92 to 106 in myelin oligodendrocyte glycoprotein (MOG) from mice and rats. Mice subjected to MOG (92–106)-induced experimental autoimmune encephalomyelitis show substantial B cell reactivity to secondary myelin antigens. Although this MOG fragment elicits only modest T cell responses, the resultant autoimmunity is profoundly severe. The peptide demonstrates encephalitogenic properties in various species, including SJL mice, DA rats, and rhesus monkeys.

MOG peptide (35-55) rat, a segment of myelin oligodendrocyte glycoprotein (MOG), exhibits encephalitogenic properties [1].

Myelin Oligodendrocyte Glycoprotein (40-54), Rat, Mouse (MOG (40-54)) is a self-antigenic epitope associated with the CD8 class of proteins within the MOG protein, presented in conjunction with H-2Db [1].

Homoglutathione, a tripeptide essential in eukaryotes, plays multifaceted roles in cellular redox regulation and exhibits taste-modifying effects [1] [2].

[Leu144,Arg147]-PLP (139-151) is a mutated fragment of the myelin proteolipid protein (PLP), featuring substitutions of tryptophan to leucine and histidine to arginine at positions 144 and 147, respectively. Immunizing mice with this peptide (50 µg) mixed in complete Freund’s adjuvant (CFA) elevates IL-4 levels in the spleen. While it suppresses Th1 cell activation in vitro, it does not do so in vivo; instead, it promotes the development of regulatory T cells. Preimmunization with [Leu144, Arg147]-PLP (139-151) postpones the onset of experimental autoimmune encephalomyelitis (EAE) triggered by encephalitogenic peptides from PLP (178-191), myelin oligodendrocyte glycoprotein (MOG) (92-106), or myelin basic protein (MBP) in mice.

R 715, a bradykinin B1 receptor antagonist, inhibits contractions in isolated human umbilical cords that express bradykinin B1 receptors (pA2 = 8.49). When administered at doses of 200, 400, and 600 µg/kg, R 715 enhances latency to tail withdrawal in the tail-flick test for diabetic neuropathy mouse models induced by streptozotocin (STZ), signaling potential analgesic properties. Furthermore, at a 1 mg/kg per day dosage, it mitigates symptoms in a mouse model of experimental autoimmune encephalomyelitis (EAE) induced by MOG35-55 antigen peptide, such as reducing hind limb weakness and paralysis, improving gait symmetry, and decreasing spinal inflammation, neuron demyelination, and lesion monocyte invasion. Additionally, R 715 at 0.01 nmol/animal, administered intracerebroventricularly (i.c.v.), lowers mean arterial blood pressure and increases heart rate in spontaneously hypertensive rats, indicating cardiovascular effects.