RELM-Alpha Mouse Recombinant, His Tag
CYT-453
5µg
25µg
1mg
Catalogue number
CYT-453
Synonyms
Introduction
RELMalpha inhibits the differentiation of 3T3-L1 preadipocytes into adipocytes but has no effect on proliferation of 3T3-L1 preadipocytes. RELMalpha is able to form heterooligomers with resistin but not RELMbeta. Since RELMalpha is expressed by adipose tissue and it is a secreted factor, our findings suggest that RELMalpha may be involved in the control of the adipogenesis as well as in the process of muscle differentiation.
In the lung, RELM-alpha is induced by hypoxia and was renamed as hypoxia-induced mitogenic factor . HIMF strongly activated Akt phosphorylation. The phosphatidylinositol 3-kinase inhibitor LY294002 inhibited HIMF-activated Akt phosphorylation. It also inhibited HIMFstimulated RPSM proliferation. Thus, the PI3K/Akt pathway, at least in part, mediates the proliferative effect of HIMF. Further studies showed that HIMF had angiogenic and vasoconstrictive properties. HIMF increased pulmonary arterial pressure and vascular resistance. Further studies suggest that HIMF regulates apoptosis and may participate in lung alveolarization and maturation.
RELMalpha 抑制 3T3-L1 前脂肪细胞分化为脂肪细胞,但对 3T3-L1 前脂肪细胞的增殖没有影响。 RELMalpha 能够与抵抗素形成异源寡聚体,但不能与 RELMbeta 形成。由于 RELMalpha 由脂肪组织表达并且它是一种分泌因子,我们的研究结果表明 RELMalpha 可能参与控制脂肪生成以及肌肉分化过程。
在肺中,RELM-α是由缺氧诱导的,并被重新命名为缺氧诱导的有丝分裂因子。 HIMF 强烈激活 Akt 磷酸化。磷脂酰肌醇 3-激酶抑制剂 LY294002 抑制 HIMF 激活的 Akt 磷酸化。它还抑制 HIMF 刺激的 RPSM 增殖。因此,PI3K/Akt 通路至少部分介导了 HIMF 的增殖作用。进一步的研究表明,HIMF 具有血管生成和血管收缩特性。 HIMF 增加肺动脉压和血管阻力。进一步的研究表明,HIMF 调节细胞凋亡并可能参与肺泡化和成熟。
Description
Source
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Formulation
Solubility
Add deionized H2O and let the lyophilized pellet dissolve completely.
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