INFER
发表于 2025-3-21 19:43:58
书目名称Apoptosis影响因子(影响力)<br> http://figure.impactfactor.cn/if/?ISSN=BK0158994<br><br> <br><br>书目名称Apoptosis影响因子(影响力)学科排名<br> http://figure.impactfactor.cn/ifr/?ISSN=BK0158994<br><br> <br><br>书目名称Apoptosis网络公开度<br> http://figure.impactfactor.cn/at/?ISSN=BK0158994<br><br> <br><br>书目名称Apoptosis网络公开度学科排名<br> http://figure.impactfactor.cn/atr/?ISSN=BK0158994<br><br> <br><br>书目名称Apoptosis被引频次<br> http://figure.impactfactor.cn/tc/?ISSN=BK0158994<br><br> <br><br>书目名称Apoptosis被引频次学科排名<br> http://figure.impactfactor.cn/tcr/?ISSN=BK0158994<br><br> <br><br>书目名称Apoptosis年度引用<br> http://figure.impactfactor.cn/ii/?ISSN=BK0158994<br><br> <br><br>书目名称Apoptosis年度引用学科排名<br> http://figure.impactfactor.cn/iir/?ISSN=BK0158994<br><br> <br><br>书目名称Apoptosis读者反馈<br> http://figure.impactfactor.cn/5y/?ISSN=BK0158994<br><br> <br><br>书目名称Apoptosis读者反馈学科排名<br> http://figure.impactfactor.cn/5yr/?ISSN=BK0158994<br><br> <br><br>
Merited
发表于 2025-3-21 23:41:06
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dowagers-hump
发表于 2025-3-22 01:13:40
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上涨
发表于 2025-3-22 08:39:04
Elemente der Achten Nebengruppedependent 32Dcl3 murine myeloid cell line. 32D cells are absolutely dependent upon IL-3 for proliferation and survival,. and have no propensity for developing factor-independent growth. In the absence of IL-3, 32D cells rapidly arrest in the Gl phase of the cell cycle and eventually undergo apoptosis..
Legion
发表于 2025-3-22 10:08:38
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内行
发表于 2025-3-22 13:14:40
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碎片
发表于 2025-3-22 17:16:07
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狂热语言
发表于 2025-3-23 00:40:52
Regulation of Apoptosis in Interleukin-3-Dependent Myeloid Progenitor Cells,dependent 32Dcl3 murine myeloid cell line. 32D cells are absolutely dependent upon IL-3 for proliferation and survival,. and have no propensity for developing factor-independent growth. In the absence of IL-3, 32D cells rapidly arrest in the Gl phase of the cell cycle and eventually undergo apoptosis..
讨厌
发表于 2025-3-23 04:58:52
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加入
发表于 2025-3-23 08:15:47
Wild Type p53 Activity Contributes to Dependence on Hematopoietic Survival Factors,s found in cancer cells are typically devoid of such activities. Hence, the principal outcome of such mutations is probably the inactivation of the tumor suppressor function of wt p53. In addition, at least certain mutations may also confer a distinct gain of function., thereby possibly contributing a novel oncogenic activity to the affected cell.