다음 MAP메이트™는 통합될 수 없습니다: -다른 분석 완충용액이 필요한 MAP메이트™. -인산 특이성 및 총 MAP메이트™ 조합, 예: 총 GSK3β 및 GSK3β(Ser 9). -PanTyr 및 자리 특이성 MAP메이트™, 예: Phospho-EGF 수용체 및 phospho-STAT1(Tyr701). -단일 표적(Akt, STAT3)를 위한 1개 이상의 1 phospho-MAP메이트™. - GAPDH 및 β-Tubulin은 panTyr를 포함하는 키트 또는 MAP메이트™와 통합될 수 없습니다.
Custom Premix Selecting "Custom Premix" option means that all of the beads you have chosen will be premixed in manufacturing before the kit is sent to you.
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이 제품은 즐겨찾기에 저장되었습니다.
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패널 유형
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96-Well Plate
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다른 시약 추가 (MAP메이트 사용을 위해 완충용액과 검출 키트가 필요함)
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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
공간 절약 옵션 다수의 키트를 구매하시는 고객은 고용량 저장을 위해 키트 포장을 제거하고 비닐백에 담긴 멀티플레스 분석 구성품을 받아 저장 공간을 절약하도록 선택할 수 있습니다.
이 제품은 즐겨찾기에 저장되었습니다.
해당 제품은 고객님의 카트에 추가되었습니다.
이제 다른 키트를 사용자 지정하거나, 사전 혼합된 키트를 선택하거나, 결재하거나 또는 주문 도구를 종료할 수 있습니다.
Despite limited regeneration capacity, partial injuries to the adult mammalian spinal cord can elicit variable degrees of functional recovery, mediated at least in part by reorganization of neuronal circuitry. Underlying mechanisms are believed to include synaptic plasticity and collateral sprouting of spared axons. Because plasticity is higher in young animals, we developed a spinal cord compression (SCC) injury model in the neonatal mouse to gain insight into the potential for reorganization during early life. The model provides a platform for high-throughput assessment of functional synaptic connectivity that is also suitable for testing the functional integration of human stem and progenitor cell-derived neurons being considered for clinical cell replacement strategies. SCC was generated at T9-T11 and functional recovery was assessed using an integrated approach including video kinematics, histology, tract tracing, electrophysiology, and high-throughput optical recording of descending inputs to identified spinal neurons. Dramatic degeneration of axons and synaptic contacts was evident within 24 hours of SCC, and loss of neurons in the injured segment was evident for at least a month thereafter. Initial hindlimb paralysis was paralleled by a loss of descending inputs to lumbar motoneurons. Within 4 days of SCC and progressively thereafter, hindlimb motility began to be restored and descending inputs reappeared, but with examples of atypical synaptic connections indicating a reorganization of circuitry. One to two weeks after SCC, hindlimb motility approached sham control levels, and weight-bearing locomotion was virtually indistinguishable in SCC and sham control mice. Genetically labeled human fetal neural progenitor cells injected into the injured spinal cord survived for at least a month, integrated into the host tissue and began to differentiate morphologically. This integrative neonatal mouse model provides opportunities to explore early adaptive plasticity mechanisms underlying functional recovery as well as the capacity for human stemcell-derived neurons to integrate functionally into spinal circuits.