anti-Chloride Channel 2 (CLCN2) Antibodies

Zebrafish Chloride Channel 2 (CLCN2) interaction partners

1. Identification and characterization of the zebrafish ClC-2a/b/c chloride channel orthologs.

Mouse (Murine) Chloride Channel 2 (CLCN2) interaction partners

1. ClC-2 knockout results in less differentiated colonic crypts and increased tumorigenicity associated with colitis via dysregulation of AJ proteins.

2. High fat diet -treated mice lacking ClC-2 showed inhibited hepatic lipid accumulation via regulating lipid metabolism through decreasing sterol regulatory element binding protein (SREBP)-1c expression and its downstream targeting enzymes such as fatty acid synthase (FAS), HMG-CoA reductase (HMGCR) and acetyl-Coenzyme A carboxylase (ACCalpha).

3. Genetic ablation of ClC-2 resulted in reduced gastric gland region, reduced parietal cell number, reduced H/K ATPase, reduced tubulovesicles and reduced stimulated acid secretion.

4. 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.

5. Loss of ClC-2 is associated with increased development of DSS-induced colitis.

6. fast gate protonation was V(m) and Cl(-) independent and the equilibrium constant for closed-open transition of unprotonated channels was facilitated by elevated [Cl(-)](i) in a V(m)-dependent manner

7. The PCR data revealed the existence of two astrocytic subpopulations markedly differing in their gene expression levels for inwardly rectifying K+ channels (Kir4.1), K(2P) channels (TREK-1 and TWIK-1) and Cl- channels (ClC2).

8. ClC-2 channels are required for colonic electroneutral absorption of NaCl and KCl.

9. permeant Cl(-) ions contribute to V(m)-dependent gating of the broadly distributed ClC-2 Cl() channel.

10. GABAA receptor-mediated synaptic inputs from basket cells were modulated by ClC-2. Our data reveal a previously unknown cell type-specific regulation of intracellular chloride homeostasis in the perisomatic region of hippocampal pyramidal neurons.

11. ClC-2 reduces barrier function in normal mucosa. Ultrastructural morphology of tight junctions and myosin light chain kinase appear to be important to the function of ClC-2 in normal mucosa.

12. these findings raise the possibility that ClC-2 expression plays a subtle neuroprotective role in the aging hippocampus

13. Heterozygous nmf240 mice present with a reduced electroretinography light peak component suggests that CLCN2 is necessary for the generation of this response component.

14. we suggest a dual role for ClC-2 in neurons, providing an additional efflux pathway for chloride and constituting a substantial part of the background conductance, which regulates excitability.

15. ClC-2 is unlikely to be a candidate rescue channel in cystic fibrosis

16. activation of host ClC-2 channels participates in the altered permeability of Plasmodium-infected erythrocytes but is not required for intraerythrocytic parasite survival

17. This study concluded that Clcn2is the inward-rectifying chloride channel in duct cells, but its expression is not apparently required for the ion reabsorption or the barrier function of salivary ductal epithelium.

18. These data demonstrate a pivotal role of ClC-2 in recovery of the intestinal epithelium barrier by anchoring assembly of tight junctions following ischemic injury.

Pig (Porcine) Chloride Channel 2 (CLCN2) interaction partners

1. ClC-2-mediated intestinal Cl - secretion restores transepithelial resistance in ischemia-injured intestine.

Human Chloride Channel 2 (CLCN2) interaction partners

1. A role of anion channels in glomerulosa membrane potential determination, aldosterone production and hypertension. The mutations are the cause of a substantial fraction of early-onset primary aldosteronism.

2. CLCN2 mutations cause primary aldosteronism, this highlight the importance of chloride in aldosterone biosynthesis and CLCN2 as the foremost chloride conductor of resting glomerulosa cells.

3. The inhibitory effects of ClC-2 knockout on HBVSMC proliferation and motility were associated with inactivation of the Wnt/beta-catenin signaling pathway, as evidenced by inhibition of beta-catenin phosphorylation and nuclear translocation, and decrease of GSK-3beta phosphorylation and survivin and cyclin D1 expression.

4. Leukoencephalopathy-causing CLCN2 mutations impair chloride channel gating and trafficking.

5. ClC-2 mRNA level was significantly increased in patients with non-alcoholic steatohepatitis, which positively correlated with the plasma levels of alanine transaminase (ALT), aspartate transaminase (AST) and insulin.

6. The findings show that RGET691 of human ClC-2 (possible binding site) plays an important functional role in fatty acid activation of human ClC-2.

7. Hyperpolarization activates CLC-2 mainly by driving intracellular anions into the channel pores.

8. The extracellular domain of GlialCAM is necessary for cell junction targeting and for mediating interactions with itself or with MLC1 and ClC-2.

9. both ubiquitous (AP-1A) and epithelium-specific (AP-1B) forms of the tetrameric clathrin adaptor AP-1 are capable of carrying out basolateral sorting of ClC-2.

10. SPAK and OSR1 are powerful negative regulators of the cell volume regulatory Cl- channel ClC-2

11. Correlation between CLC-2 gene expression and the cytoskeleton in human trabecular meshwork cells.

12. Our observations substantiate the concept that ClC-2 is involved in brain ion and water homoeostasis

13. JAK2 down-regulates ClC-2 activity and thus counteracts Cl(-) exit, an effect which may impact on cell volume regulation

14. This study demonistrated that the first auxiliary subunit of ClC-2 and suggests that ClC-2 may play a role in the pathology of MLC disease.

15. ClC-2 plays an important role in the modulation of tight junctions by influencing caveolar trafficking of tight junction protein occludin.

16. Sequence analysis of CLCN2 at genomic DNA and cDNA levels in 18 megalencephalic leukoencephalopathy MLC1 mutations revealed some nucleotide changes, but they were predicted to be nonpathogenic.

17. found significant expression of ClC-2 at the apex of ciliated cells in both rat and human airways

18. a functional interaction between the ClC-2 chloride channel and the retrograde motor dynein complex.

19. ClC-2 and ClC-3 channels are specifically upregulated in glioma membranes and endow glioma cells with an enhanced ability to transport Chloride

20. activation of hClC-2 is differentially regulated by PKA at two sites