简介：Transmissiblespongiformencephalopathyorpriondiseaseistriggeredbytheconversionfromcellularprionproteintopathogenicprionprotein.Growingevidencehasconcentratedonprionproteinconfigurationchangesandtheircorrelationwithpriondiseasetransmissibilityandpathogenicity.Invivoandinvitrostudieshaveshownthatseveralcytosolicformsofprionproteinwithspecifictopologicalstructurecandestroyintracellularstabilityandcontributetoprionproteinpathogenicity.Inthisstudy,thelatestmolecularchaperonesystemassociatedwithendoplasmicreticulum-associatedproteindegradation,theendoplasmicreticulumresidentproteinquality-controlsystemandtheubiquitinationproteasomesystem,isoutlined.Themolecularchaperonesystemdirectlycorrelateswiththeprionproteindegradationpathway.Understandingthemolecularmechanismswillhelpprovideafascinatingavenueforfurtherinvestigationsonpriondiseasetreatmentandprionprotein-inducedneurodegenerativediseases.

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简介：AbstractThe chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family (CMTM) is widely expressed in the immune system. Abnormal expression of CMTM is associated with the development of various diseases. This article summarizes the relevant research on the role of the CMTM family in immune disorders. This information will increase our understanding of pathogenesis and identify promising targets for the diagnosis and treatment of autoimmune diseases. The CMTM family is highly expressed in peripheral blood mononuclear cells. CKLF1 may be involved in the development of arthritis through its interaction with C-C chemokine receptor 4. CKLF1 is associated with the pathogenesis of lupus nephritis and psoriasis. Both CMTM4 and CMTM5 are associated with the pathogenesis of systemic lupus erythematosus. CMTM1, CMTM2, CMTM3, and CMTM6 play a role in rheumatoid arthritis, systemic sclerosis, Sjögren syndrome, and anti-phospholipid syndrome, respectively. The CMTM family has been implicated in various autoimmune diseases. Further research on the mechanism of the action of CMTM family members may lead to the development of new treatment strategies for autoimmune diseases.

简介：BACKGROUND:Studieshavesuggestedthatfibronectinleucine-richtransmembraneprotein3(FLRT3)isrelatedtoinjuryandregenerationofthenervoussystem.However,theexpressionandbiologicalcharacteristicsoftheseproteinsremainpoorlyunderstood.OBJECTIVE:ToobtainFLRT3C-terminalgenefragments,toeffectivelyexpressandpurifythetargetproteins.DESIGN,TIMEANDSETTING:AnobservationalstudyofcellularandmolecularbiologywasperformedatthelaboratoryofHistologyandEmbryologyinXiangyaSchoolofMedicine,CentralSouthUniversitybetweenOctober2007andJune2008.MATERIALS:ThreeSpragueDawleyadultratswereusedtoextracttotalRNAfromratbrains.ThepGEX4T3andEscherichiacoli(E.coli)JM109werepurchasedfromPromega.E.coliBL21wasprovidedbyNovagen.METHODS:FLRT3proteincodingC-terminalDNAfragments,atalengthof786bp,wereamplifiedusingRT-PCRtechniquefromrattotalRNA.TheamplifiedproductswereclonedintotheexpressionvectorpGEX4T3.ArecombinantexpressionvectorwasthenconstructedandintroducedintoE.coliBL21.IsopropyI-D-thiogalactopyranosidewasappliedtoinduceexpressionofrecombinantGSTfusionproteins,followedbyisolation,purification,andrenaturationofinclusionbodiesthatcomprisedrecombinantproteins.Finally,thepurifiedrecombinantproteinwasobtained.MAINOUTCOMEMEASURES:DeterminationofFLRT3C-terminalDNAsequence;expressionoftargetproteinswasassayedbySDS-PAGEelectrophoresis;purifiedrecombinantproteinwasidentifiedwithWesternblotmethods.RESULTS:FLRT3proteincodingC-terminalDNAfragments,atalengthof786bp,weresuccessfullyharvestedthroughRT-PCRamplification,andwerethenclonesintotheprokaryoticexpressionvectorpGEX4T3.Theresultsofthesequencewereconsistentwiththeknowngenesequence.SDS-PAGEanalysisdemonstratedthattherewasaspecificproteinbandintherecombinantGSTfusionproteinsatarelativemolecularmassof56,600.Therecombinantproteinwasobservedintheinclusionbody,andh

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简介：AbstractAntiphospholipid syndrome (APS) is a systemic autoimmune disease defined by thrombotic or obstetrical events and persistent antiphospholipid antibodies (aPLs). Chemokine-like factor-like MARVEL transmembrane domain-containing family (CMTM) is widely expressed in the immune system and may closely related to APS. This review aimed to systematically summarize the possible effects of CMTM on APS. Publications were collected from PubMed and Web of Science databases up to August 2020. CKLF, CKLFSF, CMTM, antiphospholipid syndrome, immune cells, and immune molecules were used as search criteria. Immune cells, including neutrophil, dendritic cells (DCs), T-cells, B-cells, and inflammatory cytokines, play an important role in the development of APS. Chemokine-like factor 1 (CKLF1) has a chemotactic effect on many cells and can affect the expression of inflammatory cytokines and adhesion molecules through the nuclear factor-kB (NF-kB) pathway or mitogen-activated protein kinase (MARK) pathway. CKLF1 can participate in the maturation of DCs, T lymphocyte activation, and the activation of neutrophils through the MAPK pathway. CMTM1 may act on Annexin A2 by regulating Ca2+ signaling. CMTM2 and CMTM6 are up-regulated in neutrophils of APS patients. Some CMTM family members influence the activation and accumulation of platelets. CMTM3 and CMTM7 are binding partners of B-cell linker protein (BLNK), thereby linking B cell receptor (BCR) and activating BLNK-mediated signal transduction in B cells. Moreover, CMTM3 and CMTM7 can act on DCs and B-1a cell development, respectively. CMTM may have potential effects on the development of APS by acting on immune cells and immune molecules. Thus, CMTM may act as a novel prognostic factor or immunomodulatory treatment option of APS.