Disease relevance of Ssg1

• CONCLUSIONS: TNBS-induced colitis alters myenteric nerve function at inflamed and noninflamed sites via a steroid-sensitive and interleukin 1-mediated process that does not require T lymphocytes [1].
• Here we describe the characteristics of an IEC-18 cell line in which the activated human H-ras gene has been introduced under the control of the steroid-sensitive promoter of the mouse mammary tumor virus long-terminal repeat [2].
• BACKGROUND: An uncharacterized circulating factor that increases vascular permeability has previously been described in childhood steroid-sensitive nephrotic syndrome (SSNS) [3].
• Rat C6 glioma cells were subcloned to produce four different cell lines (CL1, CL2, CL3 and CL4) differing in growth, differentiation and morphology: CL1 cells were slow-growing with an astrocytic appearance whereas CL4 cells grew rapidly and were small and spindle-shaped [4].
• Circulating vascular endothelial growth factor is not increased during relapses of steroid-sensitive nephrotic syndrome [3].

Psychiatry related information on Ssg1

• Thus, the present study adds novel evidence further supporting that the BNST and the central nucleus of the amygdala form part of an adrenal steroid-sensitive extrahypothalamic circuit that has been involved in fear and anxiety responses and in clinical syndromes such as melancholic depression, posttraumatic stress disorders, and addiction [5].

High impact information on Ssg1

• The posterodorsal part of the medial nucleus of the amygdala (MeAp) receives its major sensory input from the accessory olfactory bulb and projects massively to the medial preoptic nucleus and other sexually dimorphic hypothalamic nuclei thought to play key roles in mediating steroid-sensitive reproductive functions [6].
• In this study, we used laser-scanning microscopy to demonstrate that estrogen treatment induces the translocation of mu-OR immunoreactivity (mu-ORi) from the membrane to an internal location in steroid-sensitive cell groups of the limbic system and hypothalamus [7].
• We conclude that RINm5F cells show steroid-sensitive plasticity and express NPY after dexamethasone treatment concomitantly with a decreased insulin secretion and impaired increase in cytosolic Ca2+ upon depolarization with KCl or stimulation with D-glyceraldehyde [8].
• Finally, CL2 gene expression was drastically downregulated in human thyroid neoplastic cell lines and tissues [9].
• We have previously demonstrated increased NF-kappaB pathway activation in a steroid-sensitive animal model of lipopolysaccharide (LPS)-driven airway inflammation [10].

Chemical compound and disease context of Ssg1

• Namely, the maximum cortisol-binding ability was seen on a 5 day old granuloma which is the so called 'steroid sensitive stage'. Thereafter, the binding ability decreased with the increasing stage of granuloma [11].

Biological context of Ssg1

• These results indicate that the sex difference in the steroid-sensitive AVP pathways depends on other factors besides circulating hormone levels in adulthood [12].
• Inputs to the MPOA arise from several areas within the brainstem, synapsing preferentially onto steroid sensitive MPOA cells which are activated during sexual activity [13].
• The SNB/BC is a sexually dimorphic, steroid-sensitive neuromuscular system, which is critically important in male reproductive behavior [14].
• The amygdala expresses gonadal steroid-sensitive oxytocin binding sites in both the central and medial sub-nuclei, although the densities markedly differ between these nuclei [15].
• The bronchoconstriction was accompanied by a steroid-sensitive increase in cyclooxygenase (COX)-2 mRNA expression and thromboxane formation [16].

Anatomical context of Ssg1

• We report the cloning of a novel gene [steroid-sensitive gene 1 (SSG1)] that is regulated by E(2) in the rat uterus and mammary gland [17].
• The presence of VGLUT2 mRNA in steroid-sensitive regions of the hypothalamus, such as the anteroventral periventricular, paraventricular, or ventromedial nuclei indicates that gonadal and adrenal steroid can directly alter the functions of these glutamatergic neurons [18].
• Since parvocellular but not magnocellular neurons of the paraventricular nucleus have been demonstrated to be steroid sensitive in immunohistochemical studies, we suggest CRF may act directly or indirectly upon magnocellular neurons to increase OT release [19].
• Plasma ACTH, corticosteroid-binding globulin (CBG), and thymus weight were measured in the morning or evening, and these steroid-sensitive end points were related to the circulating concentrations of B (total B - CBG-bound B), total DEX, and total ALDO [20].
• The rat lumbar spinal cord contains the steroid-sensitive spinal nucleus of the bulbocavernosus (SNB), whose motoneurons innervate perineal muscles involved in copulatory reflexes [21].

Associations of Ssg1 with chemical compounds

• Steroid manipulations produced the expected changes in reproductive behaviors and steroid-sensitive organs [22].
• Vasopressin (VP) neurons in the bed nucleus of the stria terminalis (BNST) are steroid sensitive and sexually dimorphic [23].
• Dendritic retraction is also steroid sensitive and can be prevented by testosterone treatment, but is unaffected by aromatase inhibition [24].
• Steroid-sensitive gene-1 is an androgen-regulated gene expressed in prostatic smooth muscle cells in vivo [25].
• Excretion of AL CL2 occurred primarily via the kidneys and was prolonged with respect to that of free CS2 [26].

Co-localisations of Ssg1

• GAL is extensively colocalized within these steroid-sensitive cell groups where its expression is upregulated by gonadal hormones [27].

Other interactions of Ssg1

• In conjunction with previous evidence that the perinuclear zone GABA neurones are an important source of GABA terminals in the SON, these results provide a morphological basis for the hypothesis that perinuclear zone GABA neurones may be part of a steroid-sensitive neural circuitry transmitting oestrogen input to oxytocin neurones in the SON [28].
• Furthermore the data demonstrates a steroid-sensitive stress mediated increase in proenkephalin A mRNA which provides additional evidence for a role of the endogenous opiates in the hypothalamic neuroendocrine response to stress [29].

Analytical, diagnostic and therapeutic context of Ssg1

• Pituitary enlargement due to facilitation of oestrogen-induced pituitary growth may become a focus of attention when this or similar antigestagenic drugs are being used for prolonged periods in clinical trials, e.g. for limiting steroid-sensitive tumour growth [30].
• The corticosteroid effect on circulating lymphocytes in a steroid-sensitive species (rat) was studied by immunofluorescence [31].

References