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The protein encoded by HEPACAM is a single-pass type I membrane protein that localizes to the cytoplasmic side of the cell membrane. 再加上，我们可以发Hepatic and Glial Cell Adhesion Molecule 抗体 (55) 和 Hepatic and Glial Cell Adhesion Molecule 蛋白 (11)和数多这个蛋白质的别的产品。
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hepaCAM associates with connexin 43 (显示 GJA1 ELISA试剂盒), a main component of gap junctions, and enhances connexin 43 (显示 GJA1 ELISA试剂盒) localization to the plasma membrane at cellular junctions.
this study revealed that hepaCAM was downregulated in CRC (显示 CALR ELISA试剂盒) tissues and cell lines. Overexpression of hepaCAM inhibited CRC (显示 CALR ELISA试剂盒) cell proliferation, migration, and invasion in vitro. Furthermore, the tumorigenesis assay showed that increased expression of hepaCAM suppressed CRC (显示 CALR ELISA试剂盒) tumor growth and metastasis in vivo.
In a group of Egyptian patients with megalencephalic leukoencephalopathy, novel mutations were identified in HEPACAM.
DNMT1 (显示 DNMT1 ELISA试剂盒) up-regulation induced by IL-6 (显示 IL6 ELISA试剂盒)/STAT3 (显示 STAT3 ELISA试剂盒) signaling was indispensable for IL-6 (显示 IL6 ELISA试剂盒)-mediated hepaCAM loss in renal cell carcinoma (RCC (显示 XRCC1 ELISA试剂盒)) cell lines ACHN and 769-P, while DNMT3b (显示 DNMT3B ELISA试剂盒) up-regulation was crucial for hepaCAM loss in A498.
Out of 20 patients, macrocephaly, classic MRI features, motor development delay and cognitive impairment were detected in 20(100%), 20(100%), 17(85%) and 4(20%) patients, respectively. 20(100%) were clinically diagnosed with MLC. 19(95%) were genetically diagnosed with 10 novel mutations in MLC1, MLC1 and GlialCAM mutations were identified in 15 and 4 patients, respectively
HepaCAM depletion was discovered in bladder cancer tissues compared with adjacent normal tissues, and the decreased level was associated with the degradation of FoxO3.
HepaCAM proteins were significantly decreased in bladder carcinoma. Low hepaCAM was not statistically associated with clinicopathological characteristics of the patients. HepaCAM overexpression activated caspase 3 (显示 CASP3 ELISA试剂盒)/8/9, downregulated poly-ADP ribose polymerase (显示 PARP1 ELISA试剂盒) and p-SMAD2 (显示 SMAD2 ELISA试剂盒)/3, and decreased apoptosis.
The suppressive roles of HEPACAM in NSCLC.
Due to the ability to reactivate expression of hepaCAM and inhibit growth of bladder cancer cells, AZAC may represent an effective treatment for bladder cancer.
The extracellular domain of GlialCAM is necessary for cell junction targeting and for mediating interactions with itself or with MLC1 and ClC-2.
we demonstrate an evolutionary conserved role for MLC1 in regulating glial surface levels of GLIALCAM, and this interrelationship explains why patients with mutations in either gene (MLC1 or GLIALCAM) share the same clinical phenotype.
Data indicate that membrane protein MLC1 is crucial for proper localization of adhesion molecule GlialCAM and chloride channel ClC-2, and for changing ClC-2 currents.
GlialCAM, an immunoglobulin-like cell adhesion molecule (显示 MCAM ELISA试剂盒) is expressed in glial cells of the central nervous system.
The protein encoded by this gene is a single-pass type I membrane protein that localizes to the cytoplasmic side of the cell membrane. The encoded protein acts as a homodimer and is involved in cell motility and cell-matrix interactions. The expression of this gene is downregulated or undetectable in many cancer cell lines, so this may be a tumor suppressor gene.
hepatocyte cell adhesion molecule
, protein hepaCAM