The application of peptides rationally designed therapy (TP) can improve the outcome of cancer treatment. This peptide hold the potential to directly target and stimulate proliferation pathways arrest or cell death pathways. Elastin like polypeptide (ELP) is a biopolymer derived elastin which undergoes a phase transition thermal mediated.
This study using p50, a nuclear localization sequence derived peptide that inhibits the activation of NF and is involved in cancer cell survival and metastasis. In order to effectively delivery of p50, the conjugation SynB1-ELP1, thermally responsive macromolecular carrier. By applying an external heat source, lightly Hyperthermic conditions (41 ° C) to induce aggregation and therefore can be used to specifically target the ELP for solid tumors in cancer therapy.
The addition of cell penetrating peptides (the CPP) with the N-terminus of the carrier macromolecule improving cellular uptake and direct the subcellular localization of bioactive peptides. Novel TP, p50, inhibit proliferation and induce apoptosis of breast cancer cells by blocking imports of intranuclear NF. By expanding the repertoire of oncogenic targets, CPP, and the size of the ELP carrier, based on ELP polypeptide may be modulated to optimize the delivery of new therapies and allow for flexibility to create individualized cancer therapy.
Thermally Targeted p50 Peptide Inhibits Proliferation and Induces Apoptosis of Breast Cancer Cell Lines
Upregulation of miR-133a-3p in the sciatic nerve Contribute to Development of Neuropathic Pain
Micro (mi) RNAs expressed in the sciatic nerve of streptozotocin (STZ) -induced diabetic rats were evaluated in terms of potential therapies in patients with diabetic neuropathic pain (DNP). Relative miRNA expression in the sciatic nerve with DNP analyzed using next-generation sequencing and quantitative PCR. potential downstream target miRNAs allegedly using Ingenuity Pathway Analysis and TargetScan database.
In vitro experiments were performed using Schwann cells RSC96 miR-133a-3p-transfected. We do blotting and immunofluorescence analysis of micro-West and West to verify the role of miR-133a-3p. In vivo, the relationship between miR-133a-3p with DNP analyzed through AAV-miR-133a-3p intraneural (intra-epineural but extrafascicular) injection into the sciatic nerve of normal mice or injection of miR-133a-3p antagomir to the sciatic nerve of diabetes mellitus ( DM) rats.
miR-133a-3p mimics transfected into Schwann cells RSC96 increased VEGFR-2, p38α MAPK, TRAF-6, and the expression of p50 NF PIAS3 and reduce MKP3 and expression. In normal rats, AAV-miR-133a-3p delivery through intraneural injection into sciatic nerve induced mechanical allodynia and p-p38 MAPK activation. At DM rats, administration of miR-133a-3p antagomir alleviated DNP and downregulated p-p38 phosphorylation. Overexpression of miR-133a-3p on the pain induced by sciatic nerve. We suggest that miR-133a-3p is a potential therapeutic target for DNP.
Immunoregulatory effects and mechanisms of immunological response of Craterellus cornucopioides (L.) Pers. polysaccharides (CCP) with a triple-helix structure in peritoneal macrophages was investigated in vitro for the first time. This study showed that treatment of peritoneal macrophages with 80 ug / mL PKC for 48 hours significantly strengthen their phagocytic function and increased activity of lysozyme (LZM), acid phosphatase (ACP) and succinodehydrogenase (SDH) when compared to the untreated group.
Description: A sandwich quantitative ELISA assay kit for detection of Human NFKB Repressing Factor (NKRF) in samples from tissue homogenates or other biological fluids.
Description: A sandwich quantitative ELISA assay kit for detection of Human NFKB Repressing Factor (NKRF) in samples from tissue homogenates or other biological fluids.
Furthermore, Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) assay showed that 80 ug / mL PKC activated macrophages, significantly increased the mRNA expression of cytokines (IL-8, IL-1β, IFN-α and TNF-α ) and upregulated the expression of TLR4 cell membrane receptor protein, and protein kinase downstream product (MyD88, TAK1, P-IKKα / β, and P-MEK) via activation of TLR4-NF in peritoneal macrophages.
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