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The protein encoded by CEND1 is a neuron-specific protein. 再加上，我们可以发Cell Cycle Exit and Neuronal Differentiation 1 蛋白 (6)和数多这个蛋白质的别的产品。
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The detection of ALT, AFP (显示 AFP 抗体), AFP (显示 AFP 抗体)-L3, and GP73 (显示 GOLM1 抗体) has a certain guiding significance to predict the risk of hepatocellular carcinoma in hepatic cirrhosis patients
The mechanism of hepatocarcinogenesis and a promising blueprint for miR (显示 MLXIP 抗体)-493-5p-GP73 (显示 GOLM1 抗体) axis-oriented treatment of HCC (显示 FAM126A 抗体).
GP73 (显示 GOLM1 抗体) unglycosylation is associated with hepatocellular carcinoma cell motility and invasiveness.
The GOLPH2 (显示 GOLM1 抗体) is a novel marker for non-small-cell lung cancer.
Findings suggest that GP73 (显示 GOLM1 抗体) silencing through siRNA delivery may provide a low-toxicity therapy for the inhibition of tumor proliferation and metastasis.
Both gain- and loss-of-function studies determine that GOLM1 (显示 GOLM1 抗体) acts as a key oncogene (显示 RAB1A 抗体) by promoting HCC (显示 FAM126A 抗体) growth and metastasis.
A cytokine QTL at the NAA35 (显示 MAK10 抗体)-GOLM1 (显示 GOLM1 抗体) locus markedly modulated interleukin (IL)-6 (显示 IL6 抗体) production in response to multiple pathogens and was associated with susceptibility to candidemia.
knock-down of GP73 (显示 GOLM1 抗体) down-regulates HCV infection and replication in Huh7-MAVSR cells and primary human hepatocytes
Studies indicate that golgi membrane protein 1 (GOLM1 (显示 GOLM1 抗体)) may promote HCC (显示 FAM126A 抗体) by regulation of epidermal growth factor receptor (EGFR (显示 EGFR 抗体)) recycling, and suggest that therapeutic targeting of GOLM1 (显示 GOLM1 抗体) may be a potential strategy for combating hepatocellular carcinoma (HCC (显示 FAM126A 抗体)) metastasis.
these studies revealed that GP73 (显示 GOLM1 抗体) promotes hepatitis C virus (HCV) secretion by directly mediating the interaction of ApoE (显示 APOE 抗体) with HCV replication complex through binding with HCV NS5A.
data suggest that common reprogramming mechanisms exist driving the conversion of lineage-distant somatic cell types to neurons and reveal a critical role for CEND1 in NEUROG2 (显示 NEUROG2 抗体)-driven astrocytic reprogramming.
results suggest that functional interactions between BM88/Cend1, RanBPM and Dyrk1B (显示 DYRK1B 抗体) affect the balance between cellular proliferation and differentiation in Neuro 2a cells
This study suggested that Cend1 is involved in Ahi1 (显示 AHI1 抗体)-associated hypothalamic neuronal differentiation in early development, giving us fresh insight into the mechanism behind the delayed development in Joubert syndrome.
Our results suggest that Cend1 is required for normal cerebellar development.
Transplantation of BM88/Cend1-overexpressing neural progenitor cells exerts beneficial effects on tissue regeneration by enhancing the number of generated neurons and restricting the formation of astroglial scar, in a mouse model of cortical brain injury.
BM88 is widely expressed in the embryonic CNS and PNS, in both nestin (显示 NES 抗体)-positive neuroepithelial cells and post-mitotic betaIII-tubulin (显示 TUBB3 抗体) positive neurons.
Results implicate BM88 in the synchronization of cell cycle exit and differentiation of neuronal precursors in the developing nervous system.
BM88/Cend1 participates in cell cycle control and neuronal differentiation mechanisms during neonatal SVZ neurogenesis and becomes crucial for the transition from neuroblasts to mature neurons when reaching high levels
BM88 plays an essential role in regulating cell cycle exit and differentiation of Neuro 2a cells toward a neuronal phenotype
The protein encoded by this gene is a neuron-specific protein. The similar protein in pig enhances neuroblastoma cell differentiation in vitro and may be involved in neuronal differentiation in vivo. Multiple pseudogenes have been reported for this gene.
, cell cycle exit and neuronal differentiation protein 1
, cell cycle exit and neuronal differentiation 1