
Human CD272 (BTLA, B and T Lymphocyte Attenuator) is a member of the Immunoglobulin superfamily and has sequence homology to PD-1 and CTLA4. It is expressed on T and B lymphocytes and other hemopoetic lineages. Engagement of this molecule by its ligand, CD270(HVEM, a TNF superfamily member) can down regulate activated T and B cell responses. CD272 levels on antigen specific CD8+ T cells have been reported to decrease in viral specific, but not melanoma specific activated lines (1). Polymorphism of the CD272 molecule has been linked to rheumatoid arthritis (3).
Antibodies ANC6E9(cat #272-020) and ANC5A5(cat #372-020) each bind to a distinct epitope of CD272 and are suitable as a matched pair for EIA (see attachment).
Isotype: Murine IgG1k
Immunogen: Recombinant extracellular human CD272
Specificity: Antibody from clone ANC5A5 binds to CD272 on the cell surface of human PBMC in Flow cytometry, and to recombinant CD272-muIg (cat #542-020) in EIA.
Functional Application: Antibody ANC5A5 does not block binding of Biotinylated CD270(HVEM)-muIg(cat #531-030) to CD272-muIg in EIA, but appears to enhance this interaction.
References:
1) Derre’ L, DE Speiser, et al. (2010) J Clin Invest 120(1):157-167.
2) Otsuki N, Azuma M, et al. (2006) Biochem Biophys Res Com 344(4): 1121-1127.
3) Lin SC, Chan CH, et al. (2006) J Biomed Sci 13(6): 853-860.
4) Pasero C, D Olive, et al. (2009) Curr Mol Med 9(7): 911-927.
5) Gavrieli M, KM Murphy, et al. (2006) Adv Immunol 92: 152-185.
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第一类激素作用在靶细胞表面,并不进入细胞内部,而是与细胞膜表面特异的受体结合.这种结合使腺苷酸环化酶激活产生cAMP(一种第二信使),cAMP再去激活细胞内的一些特定系列的酶,从而引起各种生理效应.这是由E.W.Sutherland于1965年提出来的第二信使假说
第二类激素由于是脂溶性的小分子.能直接进入靶细胞,与靶细胞的细胞质中的受体分子结合成"激素-受体复合物",在一定条件下穿过核膜进入核内,与染色质上的一种酸性蛋白质相互作用,促进DNA样板转录相应的mRNA.
mRNA扩散出核膜进入细胞质,导致某种蛋白质(酶)的合成,从而引起这种激素的生理效应.
http://care.diabetesjournals.org/cgi/content/abstract/31/8/1479
OBJECTIVE—Hyperglycemiaisariskfactorformicrovascularcomplicationsandmayincreasetheriskofcardiovasculardiseaseinpatientswithtype2diabetes.ThisstudytestedtheLDLcholesterol–loweringagentcolesevelamHCl(colesevelam)asapotentialnoveltreatmentforimprovingglycemiccontrolinpatientswithtype2diabetesonsulfonylurea-basedtherapy.
RESEARCHDESIGNANDMETHODS—A26-week,randomized,double-blind,placebo-controlled,parallel-group,multicenterstudywascarriedoutbetweenAugust2004andAugust2006toevaluatetheefficacyandsafetyofcolesevelamforreducingA1Cinadultswithtype2diabeteswhoseglycemiccontrolwasinadequate(A1C7.5–9.5%)withexistingsulfonylureamonotherapyorsulfonylureaincombinationwithadditionaloralanti-diabetesagents.Intotal,461patientswererandomized(230givencolesevelam3.75g/dayand231givenplacebo).Theprimaryefficacymeasurementwasmeanplacebo-correctedchangeinA1Cfrombaselinetoweek26intheintent-to-treatpopulation(lastobservationcarriedforward).
RESULTS—Theleastsquares(LS)meanchangeinA1Cfrombaselinetoweek26was–0.32%inthecolesevelamgroupand+0.23%intheplacebogroup,resultinginatreatmentdifferenceof–0.54%(P<0.001).TheLSmeanpercentchangeinLDLcholesterolfrombaselinetoweek26was–16.1%inthecolesevelamgroupand+0.6%intheplacebogroup,resultinginatreatmentdifferenceof–16.7%(P<0.001).FurThermore,significantreductionsinfastingplasmaglucose,fructosamine,totalcholesterol,non–HDLcholesterol,andapolipoproteinBweredemonstratedinthecolesevelamrelativetoplacebogroupatweek26.
CONCLUSIONS—ColesevelamimprovedglycemiccontrolandreducedLDLcholesterollevelsinpatientswithtype2diabetesreceivingsulfonylurea-basedtherapy.

