Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P01189 (
beta-endorphin
)
21,003
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
SP-40
,40 bound to
beta-endorphin
via C-terminal non-opioid portion of
beta-endorphin
as well as S-protein (vitronectin) bound.
Beta-endorphin
bound mainly to
SP-40
,40, but not to S-protein, in the soluble membrane attack complex (SMAC, SC5b-9) of complement, because the results of autoradiography of the cross-linking experiment of SMAC with [125I]
beta-endorphin
revealed only a typical band of
SP-40
,40. The binding of
SP-40
,40 to
beta-endorphin
inhibited the binding of
beta-endorphin
to its receptor of rat brain; thus
SP-40
,40 might inhibit the biological action of
beta-endorphin
.
...
PMID:Beta-endorphin binding activity of SP-40,40. 768 89
Sulfated glycoprotein-2 (
SGP-2
or clusterin) is a complex multifunctional molecule that has been recently been implicated in neuronal degeneration and remodeling. We have shown that estradiol treatment results in a selective destruction of
beta-endorphin
neurons in the hypothalamic arcuate nucleus. We have used immunocytochemistry to determine the distribution of
SGP-2
immunoreactivity in the rat hypothalamus and to assess the effects of the estradiol-induced destruction of
beta-endorphin
neurons on
SGP-2
expression. We have found that
SGP-2
-immunopositive neurons normally occur in the medial preoptic area (MPOA), supraoptic nucleus (SON), paraventricular nucleus (PVN), dorsomedial nucleus (DM), and the lateral hypothalamic area (LHA) in both males and females. The neuropil appears free of label. Treatment with estradiol valerate results in the appearance of immunopositive punctate deposits in the neuropil in the MPOA, PVN and DM. The number and distribution of
SGP-2
-positive neurons are unaffected by estradiol treatment except in the MPOA, where there are twice as many
SGP-2
-positive neurons as in controls. These effects are precluded by treatment with vitamin E, with blocks the cytotoxic action of estradiol on
beta-endorphin
neurons. Thus, we interpret these changes as responses to the loss of
beta-endorphin
afferents.
...
PMID:The effect of estradiol-induced hypothalamic pathology on sulfated glycoprotein-2 (clusterin) expression in the hypothalamus. 903 92
