


Thisproductisfreezedried.Allwatermoleculeshavebeenremoved.

ThisantibodyisshippedwithitsantigenFREEofcharge!
- PeptideMDEEEDGAGAEESGQPRSFTQL(C),correspondingtoaminoacidresidues1-22ofratCACNA1G (Accession O54898).Intracellular,N-terminus.
- Westernblotanalysisofratbrainmembranes:1. Anti-CACNA1G(CaV3.1) Antibody(#ACC-021),(1:200).
2.Anti-CACNA1G(CaV3.1)Antibody,preincubatedwiththenegativecontrolantigen.
- ExpressionofCACNA1G inratcerebellumImmunohistochemicalstainingofratcerebellumusing Anti-CACNA1G(CaV3.1) Antibody(#ACC-021).A.CACNA1G immunoreactivity(green)appearsinthemolecularlayer.B.NuclearstainingusingDAPIasthecounterstain(blue).C.MergedimagesAandB.Mol=molecularlayer.Humanmyometrium(1:200)(Blanks,A.M. etal. (2007) J.Physiol. 581, 915.).
- Humanmyometriumcells(1:200)(Blanks,A.M. etal. (2007) J.Physiol. 581, 915.).
- 1.Serrano,J.R.etal.(1999)J.Gen.Physiol.114,185.
- 2.Perez-Reyes,E.(2003)Physiol.Rev.83,117.
- 3.Wain,H.M.etal.(2002)NucleicAcidsRes.30,169.
- 4.Andreasen,D.etal.(2000)Am.J.Physiol.279,F997.
Voltage-dependentCa2+ channelsprovideapathwayforrapidinfluxofCa2+ intocells, whichplaysacrucialroleinbothelectricalandmetabolicsignaling.1
T-typecurrentsaretransducedviachannelproteinsencodedbythreegenesthat composeasubfamilywithintheCaVchannelfamily.2-3
TheactivityofT-typechannelscontributestoseveralknownphysiologicalandpathophysiological phenomenaincludingburstfiringinneurons,pacemakingactivityintheheartandsecretionfromendocrinetissues.2 TherearethreeclonedT-typechannelisoforms.
CACNA1G(CaV3.1)andCACNA1H(CaV3.2)arewidelydistributedwhereastheexpressionofCACNA1I(CaV3.3) isrestrictedtothecentralnervoussystem.2
CACNA1GandCACNA1H arealsoexpressedinthekidney,butlittleisknownabouttheirphysiologicalrolethere.

ExpressionofCaV3.1inmousepelviskidneyjunction.
Immunohistochemicalstainingofmousekidneysectionsusing Anti-CACNA1G(CaV3.1)Antibody (#ACC-021).A.CaV3.1(purple)isdetectedinthepelviskidneyjunction(PKJ).B.HCN3staining(green),aMarkerofpacemakercells,isdetectedinthePKJ.C.SamesectionstainedforCaV3.1(red).D.MergeofBandCpanelsshowshighdegreeofco-localizationbetweenCaV3.1andHCN3.
Adaptedfrom Hurtado,R.etal. (2014)withpermissionof FederationofAmericanSocietiesforExperimentalBIOLOGy.
Anti-CACNA1G(CaV3.1)Antibody(#ACC-021)isahighlyspecificantibodydirectedagainstanepitopeoftheratCaV3.1channel.Theantibody canbeusedinwesternblot,immunocytochemistry,andimmunohistochemistryapplications.IthasbeendesignedtorecognizeCACNA1G fromhuman,rat,andmousesamples.
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鼠抗人CD3单克隆抗体针对人的CD3
CD3单克隆抗体,要看其说明书,该抗体是否识别其他生物(如大鼠)的CD3.
本试验阳性结果主要见于下列几种情况:
1.自身免疫性贫血,(IgG)型引起的溶血性贫血,本试验直接反应常呈强阳性,间接反应大多阴性,但亦可阳性。
2.药物诱发的免疫性溶血性贫血①α-甲基多巴型:直接及间接反应均阳性。②青霉素型:直接反应阳性,间接反应阴性,以上二型如以正常红细胞先与有关药物于37℃培育后再加病人血清、间接反应均为阳性。③福阿亭型:(奎宁等药物)抗体通常为IgM,偶有IgG型者,直接反应为阳性,间接反应阴性,但如用IgG抗血清做试剂则结果大部分均为阴性,但如培育时加入新鲜正常人血清(供应补体)则结果为阳性。
3.冷凝集素综合征直接反应阳性,间接反应阴性(试验需在37℃下进行)由于本病红细胞膜附着的是补体C4和C3而不是IgG或IgM,如果用抗IgG或抗IgM抗血清做试验时,则结果阴性,如以抗补体的抗血清做试验则直接反应阳性。
4.新生儿同种免疫溶血病,因Rh血型不合所致溶血病,直接及间接反应均强阳性,持续数周、换血输血后数天内可变为阴性,由于“ABO”血型不合引起的溶血病,结果常为阴性或弱阳性。
5.红细胞血型不合引起的输血反应,ABO或Rh血型不合输血,供者的红细胞被受者的血型抗体致敏,在供者被致敏的红细胞完全破坏以前,直接反应阳性,Rh阴性者如过去不曾接受过Rh阳性者的血或曾妊娠胎儿为Rh阳性者,间接反应阳性,如无上述接触,第一次输血后(Rh阳性的血),数天之内间接反应也会变为阳性。
6.其它在传染性单核细胞增多症、SLE、恶性淋巴瘤、慢性淋巴细胞白血病、癌肿、铅中毒、结节性动脉周围炎、EVan氏综合征等,病人直接反应亦可阳性,阵发性寒冷性血红蛋白尿症患者中,急性发作后用抗补体血清做试验直接反应常为阳性。展开

