In mammals, adipose tissue is an active secretory tissue that responds to mild hypothermia and as such is a genuine model to study molecular and cellular adaptive responses to cold-stress. A recent study identified a mammal-specific protein of the endoplasmic reticulum that is strongly induced in the inguinal subcutaneous white adipocyte upon exposure to cold, calsyntenin 3β (CLSTN3β). CLSTN3β regulates sympathetic innervation of thermogenic adipocytes and contributes to adaptive non-shivering thermogenesis. The calcium- and zinc-binding S100B is a downstream effector in the CLSTN3β pathways. We review, here, the literature on the transcriptional regulation of the S100b gene in adipocyte cells. We also rationalize the interactions of the S100B protein with its recognized or hypothesized intracellular (p53, ATAD3A, CYP2E1, AHNAK) and extracellular (Receptor for Advanced Glycation End products (RAGE), RPTPσ) target proteins in the context of adipocyte differentiation and adaptive thermogenesis. We highlight a chaperon-associated function for the intracellular S100B and point to functional synergies between the different intracellular S100B target proteins. A model of non-classical S100B secretion involving AHNAK/S100A10/annexin2-dependent exocytosis by the mean of exosomes is also proposed. Implications for related areas of research are noted and suggestions for future research are offered.

中文翻译：

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S100B蛋白和脂肪细胞对冷应激和适应性产热反应的伴侣：事实，假设和观点。

在哺乳动物中，脂肪组织是对轻度低温有反应的活性分泌组织，因此是研究分子和细胞对冷应激的适应性反应的真正模型。最近的一项研究确定了内质网的哺乳动物特异性蛋白，该蛋白在腹股沟皮下白色脂肪细胞中暴露于冷的钙调理素3β（CLSTN3β）后会强烈诱导。CLSTN3β调节产热脂肪细胞的交感神经，并有助于适应性的非颤抖生热作用。钙和锌结合的S100B是CLSTN3β途径中的下游效应子。我们在这里回顾了有关S100b转录调控的文献脂肪细胞中的基因 我们还合理化了S100B蛋白与其公认或假设的细胞内（p53，ATAD3A，CYP2E1，AHNAK）和细胞外（高级糖基化终产物受体（RAGE），RPTPσ）靶标蛋白在脂肪细胞分化和适应性产热中的相互作用。我们强调了细胞内S100B的伴侣相关功能，并指出了不同细胞内S100B目标蛋白之间的功能协同作用。还提出了一种通过外泌体的平均值涉及AHNAK / S100A10 / annexin2依赖性胞吐作用的非经典S100B分泌模型。指出了对相关研究领域的影响，并提供了对未来研究的建议。