Cdh1 Proteins
Hernia, Diaphragmatic
Anaphase-Promoting Complex-Cyclosome
Ubiquitin-Protein Ligase Complexes
Cadherins
Cdc20 Proteins
Carbohydrate Dehydrogenases
Apc5 Subunit, Anaphase-Promoting Complex-Cyclosome
Cell Cycle Proteins
Apc4 Subunit, Anaphase-Promoting Complex-Cyclosome
DNA Methylation
1-Pyrroline-5-Carboxylate Dehydrogenase
Apc1 Subunit, Anaphase-Promoting Complex-Cyclosome
Securin
Mitosis
Cyclin B
Ligases
Apc3 Subunit, Anaphase-Promoting Complex-Cyclosome
S-Phase Kinase-Associated Proteins
Headache Disorders
Ubiquitination
Prometaphase
Anaphase
Apc2 Subunit, Anaphase-Promoting Complex-Cyclosome
Apc11 Subunit, Anaphase-Promoting Complex-Cyclosome
Ubiquitin-Protein Ligases
Usher Syndromes
Mutation
Apc10 Subunit, Anaphase-Promoting Complex-Cyclosome
Stereocilia
Germ-Line Mutation
G1 Phase
Hair Cells, Auditory
Promoter Regions, Genetic
Cellobiose
Presbycusis
Cell Cycle
Saccharomyces cerevisiae Proteins
Fetal Diseases
Inhibitory phosphorylation of the APC regulator Hct1 is controlled by the kinase Cdc28 and the phosphatase Cdc14. (1/136)
BACKGROUND: Exit from mitosis requires inactivation of mitotic cyclin-dependent kinases (CDKs). A key mechanism of CDK inactivation is ubiquitin-mediated cyclin proteolysis, which is triggered by the late mitotic activation of a ubiquitin ligase known as the anaphase-promoting complex (APC). Activation of the APC requires its association with substoichiometric activating subunits termed Cdc20 and Hct1 (also known as Cdh1). Here, we explore the molecular function and regulation of the APC regulatory subunit Hct1 in Saccharomyces cerevisiae. RESULTS: Recombinant Hct1 activated the cyclin-ubiquitin ligase activity of APC isolated from multiple cell cycle stages. APC isolated from cells arrested in G1, or in late mitosis due to the cdc14-1 mutation, was more responsive to Hct1 than APC isolated from other stages. We found that Hct1 was phosphorylated in vivo at multiple CDK consensus sites during cell cycle stages when activity of the cyclin-dependent kinase Cdc28 is high and APC activity is low. Purified Hct1 was phosphorylated in vitro at these sites by purified Cdc28-cyclin complexes, and phosphorylation abolished the ability of Hct1 to activate the APC in vitro. The phosphatase Cdc14, which is known to be required for APC activation in vivo, was able to reverse the effects of Cdc28 by catalyzing Hct1 dephosphorylation and activation. CONCLUSIONS: We conclude that Hct1 phosphorylation is a key regulatory mechanism in the control of cyclin destruction. Phosphorylation of Hct1 provides a mechanism by which Cdc28 blocks its own inactivation during S phase and early mitosis. Following anaphase, dephosphorylation of Hct1 by Cdc14 may help initiate cyclin destruction. (+info)Pds1 and Esp1 control both anaphase and mitotic exit in normal cells and after DNA damage. (2/136)
The separation of sister chromatids in anaphase is followed by spindle disassembly and cytokinesis. These events are governed by the anaphase-promoting complex (APC), which triggers the ubiquitin-dependent proteolysis of key regulatory proteins: anaphase requires the destruction of the anaphase inhibitor Pds1, whereas mitotic exit requires the destruction of mitotic cyclins and the inactivation of Cdk1. We find that Pds1 is not only an inhibitor of anaphase, but also blocks cyclin destruction and mitotic exit by a mechanism independent of its effects on sister chromatid separation. Pds1 is also required for the mitotic arrest and inhibition of cyclin destruction that occurs after DNA damage. Even in anaphase cells, where Pds1 levels are normally low, DNA damage stabilizes Pds1 and prevents cyclin destruction and mitotic exit. Pds1 blocks cyclin destruction by inhibiting its binding partner Esp1. Mutations in ESP1 delay cyclin destruction; overexpression of ESP1 causes premature cyclin destruction in cells arrested in metaphase by spindle defects and in cells arrested in metaphase and anaphase by DNA damage. The effects of Esp1 are dependent on Cdc20 (an activating subunit of the APC) and on several additional proteins (Cdc5, Cdc14, Cdc15, Tem1) that form a regulatory network governing mitotic exit. We speculate that the inhibition of cyclin destruction by Pds1 may contribute to the ordering of late mitotic events by ensuring that mitotic exit is delayed until after anaphase is initiated. In addition, the stabilization of Pds1 after DNA damage provides a mechanism to delay both anaphase and mitotic exit while DNA repair occurs. (+info)Regulation of APC activity by phosphorylation and regulatory factors. (3/136)
Ubiquitin-dependent proteolysis of Cut2/Pds1 and Cyclin B is required for sister chromatid separation and exit from mitosis, respectively. Anaphase-promoting complex/cyclosome (APC) specifically ubiquitinates Cut2/Pds1 at metaphase-anaphase transition, and ubiquitinates Cyclin B in late mitosis and G1 phase. However, the exact regulatory mechanism of substrate-specific activation of mammalian APC with the right timing remains to be elucidated. We found that not only the binding of the activators Cdc20 and Cdh1 and the inhibitor Mad2 to APC, but also the phosphorylation of Cdc20 and Cdh1 by Cdc2-Cyclin B and that of APC by Polo-like kinase and cAMP-dependent protein kinase, regulate APC activity. The cooperation of the phosphorylation/dephosphorylation and the regulatory factors in regulation of APC activity may thus control the precise progression of mitosis. (+info)Expression of the CDH1-associated form of the anaphase-promoting complex in postmitotic neurons. (4/136)
The anaphase-promoting complex/cyclosome (APC) is a tightly cell cycle-regulated ubiquitin-protein ligase that targets cyclin B and other destruction box-containing proteins for proteolysis at the end of mitosis and in G1. Recent work has shown that activation of the APC in mitosis depends on CDC20, whereas APC is maintained active in G1 via association with the CDC20-related protein CDH1. Here we show that the mitotic activator CDC20 is the only component of the APC ubiquitination pathway whose expression is restricted to proliferating cells, whereas the APC and CDH1 are also expressed in several mammalian tissues that predominantly contain differentiated cells, such as adult brain. Immunocytochemical analyses of cultured rat hippocampal neurons and of mouse and human brain sections indicate that the APC and CDH1 are ubiquitously expressed in the nuclei of postmitotic terminally differentiated neurons. The APC purified from brain contains all core subunits known from proliferating cells and is tightly associated with CDH1. Purified brain APC(CDH1) has a high cyclin B ubiquitination activity that depends less on the destruction box than on the activity of mitotic APC(CDC20). On the basis of these results, we propose that the functions of APC(CDH1) are not restricted to controlling cell-cycle progression but may include the ubiquitination of yet unidentified substrates in differentiated cells. (+info)The mammalian Fizzy and Fizzy-related genes are regulated at the transcriptional and post-transcriptional levels. (5/136)
The cyclosome pathway of ubiquitin-mediated proteolysis plays an essential role in cell cycle control. The multisubunit cyclosome is regulated by transient interactions with Fizzy (Fzy) and Fizzy-related (Fzr) genes. We report here that both Fzy and Fzr are transcribed in a cell cycle specific but distinct manner. Fzy transcription starts after the restriction point in late G1 and ceases upon cell division. Fzr transcription also ceases upon cell division but resumes already in mid G1, before the restriction point, and takes place also in G0. Fzr has further a striking cell cycle specific pattern of mRNA stability. During most of the cell cycle its message is fairly stable, however upon exit from mitosis it is rapidly degraded. This result is puzzling because Fzr is essential for cyclosome activity in G1, and points to a complex pattern of Fzr regulation. (+info)Two different modes of cyclin clb2 proteolysis during mitosis in Saccharomyces cerevisiae. (6/136)
Sister chromatid separation and mitotic exit are triggered by the anaphase-promoting complex (APC/C) which is a multi-subunit ubiquitin ligase required for proteolytic degradation of various target proteins. Cdc20 and Cdh1 are substrate-specific activators of the APC/C. It was previously proposed that Cdh1 is essential for proteolysis of the yeast mitotic cyclin Clb2. We show that Clb2 proteolysis is triggered by two different modes during mitosis. A fraction of Clb2 is degraded during anaphase in the absence of Cdh1. However, a second fraction of Clb2 remains stable during anaphase and is degraded in a Cdh1-dependent manner as cells exit from mitosis. Most of cyclin Clb3 is degraded independently of Cdh1. Our data imply that degradation of mitotic cyclins is initiated by a Cdh1-independent mechanism. (+info)The KEN box: an APC recognition signal distinct from the D box targeted by Cdh1. (7/136)
The ordered progression through the cell cycle depends on regulating the abundance of several proteins through ubiquitin-mediated proteolysis. Degradation is precisely timed and specific. One key component of the degradation system, the anaphase promoting complex (APC), is a ubiquitin protein ligase. It is activated both during mitosis and late in mitosis/G(1), by the WD repeat proteins Cdc20 and Cdh1, respectively. These activators target distinct sets of substrates. Cdc20-APC requires a well-defined destruction box (D box), whereas Cdh1-APC confers a different and as yet unidentified specificity. We have determined the sequence specificity for Cdh1-APC using two assays, ubiquitination in a completely defined and purified system and degradation promoted by Cdh1-APC in Xenopus extracts. Cdc20 is itself a Cdh1-APC substrate. Vertebrate Cdc20 lacks a D box and therefore is recognized by Cdh1-APC through a different sequence. By analysis of Cdc20 as a substrate, we have identified a new recognition signal. This signal, composed of K-E-N, serves as a general targeting signal for Cdh1-APC. Like the D box, it is transposable to other proteins. Using the KEN box as a template, we have identified cell cycle genes Nek2 and B99 as additional Cdh1-APC substrates. Mutation in the KEN box stabilizes all three proteins against ubiquitination and degradation. (+info)Mitotic regulation of the APC activator proteins CDC20 and CDH1. (8/136)
The ordered activation of the ubiquitin protein ligase anaphase-promoting complex (APC) or cyclosome by CDC20 in metaphase and by CDH1 in telophase is essential for anaphase and for exit from mitosis, respectively. Here, we show that CDC20 can only bind to and activate the mitotically phosphorylated form of the Xenopus and the human APC in vitro. In contrast, the analysis of phosphorylated and nonphosphorylated forms of CDC20 suggests that CDC20 phosphorylation is neither sufficient nor required for APC activation. On the basis of these results and the observation that APC phosphorylation correlates with APC activation in vivo, we propose that mitotic APC phosphorylation is an important mechanism that controls the proper timing of APC(CDC20) activation. We further show that CDH1 is phosphorylated in vivo during S, G2, and M phase and that CDH1 levels fluctuate during the cell cycle. In vitro, phosphorylated CDH1 neither binds to nor activates the APC as efficiently as does nonphosphorylated CDH1. Nonphosphorylatable CDH1 mutants constitutively activate APC in vitro and in vivo, whereas mutants mimicking the phosphorylated form of CDH1 are constitutively inactive. These results suggest that mitotic kinases have antagonistic roles in regulating APC(CDC20) and APC(CDH1); the phosphorylation of APC subunits is required to allow APC activation by CDC20, whereas the phosphorylation of CDH1 prevents activation of the APC by CDH1. These mechanisms can explain the temporal order of APC activation by CDC20 and CDH1 and may help to ensure that exit from mitosis is not initiated before anaphase has occurred. (+info)Example sentences for "Hernia, Diaphragmatic" in english.
1. The baby was diagnosed with a diaphragmatic hernia at birth and underwent surgery to repair it within the first few days of life.
2. The patient experienced severe symptoms of a diaphragmatic hernia, including difficulty swallowing and recurrent vomiting, and was referred for surgical intervention.
3. The surgeon specialized in the repair of congenital diaphragmatic hernias and had successfully treated many infants with this condition.
There are several types of stomach neoplasms, including:
1. Adenocarcinoma: This is the most common type of stomach cancer, accounting for approximately 90% of all cases. It begins in the glandular cells that line the stomach and can spread to other parts of the body.
2. Squamous cell carcinoma: This type of cancer begins in the squamous cells that cover the outer layer of the stomach. It is less common than adenocarcinoma but more likely to be found in the upper part of the stomach.
3. Gastric mixed adenocarcinomasquamous cell carcinoma: This type of cancer is a combination of adenocarcinoma and squamous cell carcinoma.
4. Lymphoma: This is a cancer of the immune system that can occur in the stomach. It is less common than other types of stomach cancer but can be more aggressive.
5. Carcinomas of the stomach: These are malignant tumors that arise from the epithelial cells lining the stomach. They can be subdivided into adenocarcinoma, squamous cell carcinoma, and others.
6. Gastric brunner's gland adenoma: This is a rare type of benign tumor that arises from the Brunner's glands in the stomach.
7. Gastric polyps: These are growths that occur on the lining of the stomach and can be either benign or malignant.
The symptoms of stomach neoplasms vary depending on the location, size, and type of tumor. Common symptoms include abdominal pain, nausea, vomiting, weight loss, and difficulty swallowing. Diagnosis is usually made through a combination of endoscopy, imaging studies (such as CT or PET scans), and biopsy. Treatment depends on the type and stage of the tumor and may include surgery, chemotherapy, radiation therapy, or a combination of these. The prognosis for stomach neoplasms varies depending on the type and stage of the tumor, but early detection and treatment can improve outcomes.
Primary headache disorders are those that are not caused by another medical condition or injury, and include:
1. Migraine: a severe, debilitating headache that can last for hours or even days, often accompanied by sensitivity to light and sound, nausea, and vomiting.
2. Tension headache: a common type of headache that is often described as a dull, squeezing pain on both sides of the head.
3. Cluster headache: a rare and intense form of headache that occurs in clusters or cycles, typically lasting several weeks or months.
4. Sinus headache: a type of headache caused by inflammation or infection in the sinuses.
5. Trigeminal neuralgia: a chronic pain disorder that affects the nerves in the face and head.
Secondary headache disorders are those that are caused by another medical condition or injury, such as:
1. Medication overuse headache: a type of headache that develops as a result of taking too much pain medication.
2. Hormonal headache: a type of headache that occurs due to changes in hormone levels, such as during menstruation or menopause.
3. Headache caused by underlying medical conditions, such as stroke, tumors, or sinusitis.
4. Headache caused by trauma or injury, such as whiplash or a concussion.
Headache disorders can have a significant impact on an individual's quality of life, and can affect their ability to work, sleep, and participate in daily activities. Treatment for headache disorders depends on the underlying cause, but may include medication, lifestyle changes, and alternative therapies such as acupuncture or biofeedback.
The Usher syndromes are a group of rare genetic disorders that affect both hearing and vision. They are caused by mutations in specific genes and can be inherited in an autosomal recessive or X-linked manner. The syndromes are characterized by progressive retinal degeneration, hearing loss, and vestibular dysfunction.
Source: National Institute on Deafness and Other Communication Disorders (NIDCD)
Note: This is a medical definition, and the term "Usher Syndromes" is not commonly used in everyday conversation. It is used primarily in the medical field to describe this specific group of disorders.
There are several types of hypotrichosis, including:
1. Congenital hypotrichosis: This type is present at birth and is caused by genetic mutations.
2. Acquired hypotrichosis: This type can develop later in life due to various factors such as hormonal imbalances, nutritional deficiencies, or certain medical conditions like thyroid disorders or anemia.
3. Localized hypotrichosis: This type affects only a specific area of the body, such as the scalp or eyebrows.
4. Generalized hypotrichosis: This type affects the entire body.
Hypotrichosis can have a significant impact on an individual's self-esteem and quality of life, especially if it results in noticeable hair loss or thinning. Treatment options for hypotrichosis include medications such as minoxidil (Rogaine) and finasteride (Propecia), as well as non-medical treatments like hair transplantation and low-level laser therapy (LLLT). In some cases, hypotrichosis may be a sign of an underlying medical condition, so it is important to consult with a healthcare professional for proper diagnosis and treatment.
Presbycusis is a type of hearing loss that affects older adults and is caused by aging and wear and tear on the hearing system over time. It is a common condition that can cause difficulty hearing high-pitched sounds, understanding speech in noisy environments, and experiencing ringing or other sounds in the ears (tinnitus).
Etymology:
The term "presbycusis" comes from the Greek words "presby," meaning "elderly," and "akouo," meaning "to hear."
Synonyms: age-related hearing loss, sensorineural hearing loss, hearing impairment.
Antonyms: normal hearing, youthful hearing.
Hypernyms: hearing disorder, auditory disorder.
Hyponyms: noise-induced hearing loss, ototoxicity, Meniere's disease.
Collocations: hearing aid, cochlear implant, audiogram, hearing test.
Sentence examples:
1. The 65-year-old man experienced presbycusis and had difficulty understanding his grandchildren's voices.
2. The doctor recommended a hearing aid for the patient's presbycusis.
3. Presbycusis is a common condition in older adults and can be treated with hearing aids or cochlear implants.
Examples of fetal diseases include:
1. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21, which can cause delays in physical and intellectual development, as well as increased risk of heart defects and other health problems.
2. Spina bifida: A birth defect that affects the development of the spine and brain, resulting in a range of symptoms from mild to severe.
3. Cystic fibrosis: A genetic disorder that affects the respiratory and digestive systems, causing thick mucus buildup and recurring lung infections.
4. Anencephaly: A condition where a portion of the brain and skull are missing, which is usually fatal within a few days or weeks of birth.
5. Clubfoot: A deformity of the foot and ankle that can be treated with casts or surgery.
6. Hirschsprung's disease: A condition where the nerve cells that control bowel movements are missing, leading to constipation and other symptoms.
7. Diaphragmatic hernia: A birth defect that occurs when there is a hole in the diaphragm, allowing organs from the abdomen to move into the chest cavity.
8. Gastroschisis: A birth defect where the intestines protrude through a opening in the abdominal wall.
9. Congenital heart disease: Heart defects that are present at birth, such as holes in the heart or narrowed blood vessels.
10. Neural tube defects: Defects that affect the brain and spine, such as spina bifida and anencephaly.
Early detection and diagnosis of fetal diseases can be crucial for ensuring proper medical care and improving outcomes for affected babies. Prenatal testing, such as ultrasound and blood tests, can help identify fetal anomalies and genetic disorders during pregnancy.
Cadherin
Hereditary diffuse gastric cancer
Cdc14
Cadherin-1
ANAPC7
ANAPC4
ANAPC11
CDC16
ANAPC2
ANAPC10
ANAPC5
CDC20
CKAP2
FZR1
ANAPC1
40S ribosomal protein S27a
FOXM1
STAU1
CDH3 (gene)
Anaphase-promoting complex
CDC27
CDC23
Clb 5,6 (Cdk1)
FBXO5
SCF complex
CDH16
Plakoglobin
Biochemical switches in the cell cycle
Mitotic exit
CpG island hypermethylation
Signet ring cell carcinoma
Pharmacoepigenetics
NEDD9
P120 (protein)
CHD1
PTPRK
List of OMIM disorder codes
FYN
SKP2
Angelika Amon
Catenin beta-1
Telophase
Hereditary lobular breast cancer
Neurogenetics
C-Met
PFKFB3
BUB1
PTPRM
Histone deacetylase 2
CDH1 gene: MedlinePlus Genetics
AmotL2 disrupts apical-basal cell polarity and promotes tumour invasion | Nature Communications
IJMS | Free Full-Text | Characterizing Metastatic HER2-Positive Gastric Cancer at the CDH1 Haplotype
AREB6 Antibody - N-terminal region (P100657 T100) | Aviva Systems Biology | Aviva Systems Biology
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DeCS
Stomach: Adenocarcinoma Imaging Pearls - Educational Tools | CT Scanning | CT Imaging | CT Scan Protocols - CTisus
WHO EMRO | Gastric cancer in the Arab World: a systematic review | Volume 28 issue 7 | EMHJ volume 28 2022
Pirofosfatases/metabolismo
E-cadherin Antibody | Affinity Biosciences
APC - Everything2.com
LEM-domain proteins are lost during human spermiogenesis but BAF and BAF-L persist in: Reproduction Volume 154 Issue 4 (2017)
Human Genome Epidemiology Literature Finder|Home|PHGKB
Identification of β-catenin-interacting proteins in nuclear fractions of native rat collecting duct cells<...
FAQs - The Lobular Breast Cancer Alliance
Multifocal gastric adenocarcinoma in a patient with LRBA deficiency | Orphanet Journal of Rare Diseases | Full Text
Ras相关结构域家族成员5对头颈鳞
Snail1a and Snail1b cooperate in the anterior migration of the axial mesendoderm in the zebrafish embryo | Development | The...
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Immunotherapy with defense checkpoint inhibitors offers opened a fresh arena in - High potency inhibitors of MDM2 pathway
EBV persistence in gastric cancer cases conventionally classified as EBER-ISH negative | Infectious Agents and Cancer | Full...
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HIT-result
sia2 Summary
Dr Chiara Bardella - Institute of Cancer and Genomic Sciences - University of Birmingham
CDC20 and CDH13
- 6. Mitotic regulation of the APC activator proteins CDC20 and CDH1. (nih.gov)
- These are known as Cdc20 and Cdh1 . (everything2.com)
- This is mediated by the specificty factors Cdc20 and Cdh1 in late mitosis, and by Cdh1 in G1. (everything2.com)
Antigen1
- Cadherin-1 (CDH1) is also known as epithelial cadherin (E-cadherin), CD_antigen (CD324), Uvomorulin (UVO) ECAD and CDHE, CDH1 / CD324 contains 5 cadherin domains. (acrobiosystems.com)
Peptides3
- We offer FZR1/CDH1 Peptides and FZR1/CDH1 Proteins for use in common research applications: Blocking/Neutralizing, Control, ELISA, Immunoprecipitation, Protein Array, Western Blot. (novusbio.com)
- Our FZR1/CDH1 Peptides and FZR1/CDH1 Proteins can be used in a variety of model species: Human. (novusbio.com)
- Choose from our FZR1/CDH1 Peptides and Proteins. (novusbio.com)
Kinase2
- 19. Phosphorylation of ICBP90 by protein kinase A enhances topoisomerase IIalpha expression. (nih.gov)
- RESULT: In Enpp1-/- knee joints, we found significant chondrocyte apoptosis and proteomic results showed that abnormal expression of AMP-activated protein kinase (AMPK) signaling pathway may contribute to this phenotype. (bvsalud.org)
Western Blot1
- WB: For western blot detection of denatured protein samples. (affbiotech.com)
Genes2
- 14. Expression Profiles of the Phosphatase and Tensin Homolog (PTEN), CDH1, and CDH2 Genes, and the Cell Membrane Protein, CD133, in the Ishikawa Human Endometrial Adenocarcinoma Cell Line. (nih.gov)
- As a proof-of-concept, we applied PMEA to two breast cancer datasets: TCGA and METABRIC and identified several genes, such as GATA3, PIK3CA, MAP3K1, CDH1 and CBFB, whose mutations are significantly mutually exclusive to p53 mutations. (nih.gov)
Hereditary Diffuse Gastric Cancer2
- More than 120 inherited mutations in the CDH1 gene have been found to cause a familial cancer disorder called hereditary diffuse gastric cancer (HDGC). (medlineplus.gov)
- Defects in CDH1 / CD324 / ECAD are the cause of hereditary diffuse gastric cancer (HDGC). (acrobiosystems.com)
Cadherin14
- The CDH1 gene provides instructions for making a protein called epithelial cadherin or E-cadherin. (medlineplus.gov)
- E-cadherin belongs to a family of proteins called cadherins whose function is to help neighboring cells stick to one another (cell adhesion) to form organized tissues. (medlineplus.gov)
- Another protein called p120-catenin, produced from the CTNND1 gene, helps keep E-cadherin in its proper place in the cell membrane, preventing it from being taken into the cell through a process called endocytosis and broken down prematurely. (medlineplus.gov)
- E-cadherin is one of the best-understood cadherin proteins. (medlineplus.gov)
- Interactions between the E-cadherin and p120-catenin proteins, in particular, are thought to be important for normal development of the head and face (craniofacial development), including the eyelids and teeth. (medlineplus.gov)
- E-cadherin also acts as a tumor suppressor protein, which means it prevents cells from growing and dividing too rapidly or in an uncontrolled way. (medlineplus.gov)
- Researchers believe that the resulting loss of E-cadherin protein may allow breast cells to grow and divide unchecked, leading to a cancerous tumor. (medlineplus.gov)
- The mutations that cause HDGC often lead to the production of an abnormally short, nonfunctional version of the E-cadherin protein or lead to the production of a protein with an altered structure. (medlineplus.gov)
- CDH1 gene mutations that cause BCD syndrome are thought to result in an abnormal E-cadherin protein that is quickly broken down. (medlineplus.gov)
- A shortage of E-cadherin protein impairs the interaction between E-cadherin and p120-catenin and affects craniofacial development, leading to the features of BCD syndrome. (medlineplus.gov)
- The encoded protein is a calcium dependent cell-cell adhesion glycoprotein comprised of five extracellular cadherin repeats, a transmembrane region and a highly conserved cytoplasmic tail. (affbiotech.com)
- The purity of Human E-Cadherin (155-709) Protein, Fc Tag (Cat. (acrobiosystems.com)
- In ILC, the inability of cells to stick together is due to the loss of a functioning protein called E-cadherin. (lobularbreastcancer.org)
- 4, 5 Loss of E-cadherin is often due to an inactivating mutation in the CDH1 gene. (lobularbreastcancer.org)
Mutations8
- Inherited mutations in the CDH1 gene increase a woman's risk of developing a form of breast cancer that begins in the milk-producing glands (lobular breast cancer). (medlineplus.gov)
- Inherited mutations in the CDH1 gene are thought to account for only a small fraction of all breast cancer cases. (medlineplus.gov)
- CDH1 gene mutations also occur commonly in lobular breast cancers in women without a family history of the disease. (medlineplus.gov)
- People with CDH1 gene mutations associated with HDGC have a 56 to 70 percent chance of developing stomach (gastric) cancer in their lifetimes. (medlineplus.gov)
- People with HDGC caused by CDH1 gene mutations are born with one mutated copy of the gene in each cell. (medlineplus.gov)
- At least five inherited CDH1 gene mutations have been identified in people with blepharocheilodontic (BCD) syndrome. (medlineplus.gov)
- Despite the association of CDH1 gene mutations with increased cancer risk (see below), it is unclear whether people with BCD syndrome are at increased risk of developing cancer. (medlineplus.gov)
- denoting the phosphorylated overall: congenital download data mining and predictive analysis intelligence mutations bond with proteins who generate with a metabolism with a other Expression. (evakoch.com)
CD3241
- CDH1 / CD324 / ECAD is expressed in non-neural epithelial tissues. (acrobiosystems.com)
Family of proteins1
- 3. ICBP90 belongs to a new family of proteins with an expression that is deregulated in cancer cells. (nih.gov)
Activator1
- Cdh1 is an activator of the anaphase-promoting complex-cyclosome and is involved in substrate recognition. (nih.gov)
Pathways2
- We believe that determining the mechanisms by which enzymes transfer Ubls will be of broad importance, much like studies of protein kinases have influenced our knowledge of signaling pathways and their roles in diseases. (stjude.org)
- multiple cross-links are organic in often all normal surfaces where they suffer acylated first pathways been on their G-protein download data mining and predictive analysis intelligence gathering and. (evakoch.com)
Mediates3
- The ectodomain of this protein mediates bacterial adhesion to mammalian cells and the cytoplasmic domain is required for internalization. (affbiotech.com)
- Substrate recognition component of a SCF (SKP1-CUL1-F-box protein) E3 ubiquitin-protein ligase complex which mediates the ubiquitination and subsequent proteasomal degradation of target proteins involved in cell cycle progression, signal transduction and transcription. (nih.gov)
- iota of ERCC6 heterotrimer due of NOTCH3 mediates to activation of increase proteins in catalytic mechanisms leading NICD3( Talora et al. (erik-mill.de)
PTEN2
- Nuclear PTEN is now known to serve lipid-phosphatase-independent functions in regulating the cell cycle by promoting acetylation of p53 and upregulating RAD51 in response to DNA damage [3], and by mediating APC/C tumor suppression by promoting association with the adaptor CDH1 [4]. (careersfromscience.org)
- They showed a direct interaction of PTEN with S6K and suggested this is mediated by the master nuclear export protein Crm1. (careersfromscience.org)
Induces1
- 33) and the apical receptors of the Fourier protein, the world associated to work induces well viable in some processes of transcription energy. (evakoch.com)
Expression3
- Transcription Factor AREB6 / transcription factor 8 /zinc finger homeodomain enhancer-binding protein inhibits interleukin-2 (IL-2) gene expression. (avivasysbio.com)
- expression cross-links are proven in a universal hydrolysis of Kainate primary functions, comprising Transport as adaptors, cities or CDH1 receptors. (evakoch.com)
- A cytotoxic T-lymphocyte associated protein 4 (CTLA4) expression in T lymphocytes was determined by flow cytometry. (biomedcentral.com)
Antibody1
- CDH1 antibody detects endogenous levels of total CDH1. (affbiotech.com)
Ubiquitin5
- The Schulman lab studies the structural basis for post-translational modification by ubiquitin and ubiquitin-like proteins (Ubls). (stjude.org)
- Structure of a RING E3 trapped in action reveals ligation mechanism for the ubiquitin-like protein NEDD8. (stjude.org)
- Dynamic regulation of macroautophagy by distinctive ubiquitin-like proteins. (stjude.org)
- Ubiquitin ligases promote regulated proteolysis (protein degradation) by attaching chains of a small protein called ubiquitin to target proteins, which causes their degradation. (everything2.com)
- Through the ubiquitin-mediated proteasomal degradation of hepatitis C virus non-structural protein 5A, has an antiviral activity towards that virus. (nih.gov)
Substrate2
- 18. Hematopoietic PBX-interacting protein is a substrate and an inhibitor of the APC/C-Cdc20 complex and regulates mitosis by stabilizing cyclin B1. (nih.gov)
- The APC has two major mitotic substrate specificity factors that target different proteins for degradation at different times in the cell cycle. (everything2.com)
Chromatin2
- In somatic cells, interactions between the NL and the chromatin have been demonstrated: LEM-domain proteins and LBR interact with the NL and respectively, the chromatin proteins BAF and HP1. (bioscientifica.com)
- We therefore sought to characterise the lamina-chromatin interface during spermiogenesis, by investigating the localisation of six LEM-domain proteins, two BAF proteins and LBR, in human spermatids and spermatozoa. (bioscientifica.com)
Cadherins1
- Cadherins are calcium-dependent cell adhesion proteins. (affbiotech.com)
Extracellular1
- NOTCH3, through tandem resulting, links codon of the RNA extracellular PC HuD, which is resulting of IKZF1 into pathophysiological protein-bound kinases. (erik-mill.de)
Interactions2
- However, different Ubls alter the functions of their targets in different ways, such as by changing the target's subcellular localization, enzymatic activity, or interactions with other proteins or DNA. (stjude.org)
- lipid of interactions bacterial of urban science Constructing hormones to homolog of the acid length TAL1, transcription of the TAL1: COPI-independent biosynthesis, and energy of cyclin D1( CCND1) conduction, which is chain protein( Talora et al. (erik-mill.de)
Phosphorylation2
- In the renal collecting duct, vasopressin stimulates the nuclear translocation and phosphorylation (at Ser 552 ) of β-catenin, a multifunctional protein that acts as a transcriptional coregulator in the nucleus. (johnshopkins.edu)
- In the renal collecting duct, vasopressin stimulates the nuclear translocation and phosphorylation (at Ser552) of β-catenin, a multifunctional protein that acts as a transcriptional coregulator in the nucleus. (johnshopkins.edu)
Mutation1
- An additional mutation that impairs the normal copy of the CDH1 gene is needed for cancer to develop. (medlineplus.gov)
Regulation1
- The purpose of this study was to identify β-catenin-interacting proteins that might be involved in transcriptional regulation in rat inner medullary collecting duct (IMCD) cells, using experimental and computational approaches. (johnshopkins.edu)
Apical1
- The establishment and the maintenance of apical-basal cell polarity and eventually the depolarization of a cell is a complex process controlled by a set of core protein complexes. (nature.com)
Membrane1
- This protein is found within the membrane that surrounds epithelial cells, which are the cells that line the surfaces and cavities of the body, such as the inside of the eyelids and mouth. (medlineplus.gov)
Mutually1
- The evolutionary conserved proteins localize asymmetrically before morphological polarization and mutually antagonize each other 5 . (nature.com)
Molecular Weight1
- No. ECD-H5256) is more than 90% and the molecular weight of this protein is around 200-230 kDa verified by SEC-MALS. (acrobiosystems.com)
Nuclear1
- In spermatids, no protein localised to the nuclear periphery, but five were nucleoplasmic, receding towards the posterior nuclear pole as spermatids matured. (bioscientifica.com)
Mitotic1
- 19. The checkpoint protein MAD2 and the mitotic regulator CDC20 form a ternary complex with the anaphase-promoting complex to control anaphase initiation. (nih.gov)
Activation1
- More protein tracts have to be said and reviewed in the activation. (erik-mill.de)
Mechanisms1
- CDH1 / E-CAD is involved in mechanisms regulating cell-cell adhesions, mobility and proliferation of epithelial cells and has a potent invasive suppressor role. (acrobiosystems.com)
Targets3
- Post-translational covalent attachment of Ubls to protein targets is a primary eukaryotic regulatory mechanism. (stjude.org)
- Ubls are attached to protein targets by a series of molecular handoffs involving an E1 activating enzyme, an E2 conjugating enzyme (or Ubc), an E3 ligase, and the target. (stjude.org)
- The APC targets a protein known as securin for degradation. (everything2.com)
Promoter1
- Influence of HRH2 promoter polymorphism on aberrant DNA methylation of DAPK and CDH1 in the gastric epithelium. (cdc.gov)
Human2
- Electron microscopy structure of human APC/C(CDH1)-EMI1 reveals multimodal mechanism of E3 ligase shutdown. (stjude.org)
- Purified recombinant fragment of human CDH1 expressed in E. Coli. (affbiotech.com)
Synthase1
- Briefly, upon binding DNA, the protein cGAS (cyclic GMP-AMP Synthase) triggers reaction of GTP and ATP to form cGAMP. (cmvpromotor.com)
Inhibitor1
- Securin is an inhibitor of the protease called separase that cleaves a protein called cohesisn , which holds sister chromatids together. (everything2.com)
Manner1
- Promotes ubiquitination and destruction of CDH1 in a CK1-Dependent Manner, thereby regulating cell migration. (nih.gov)
Data1
- Over 150 enzymes contain known removed in proteins, and Similarly a download data mining and predictive analysis intelligence of these is located found. (evakoch.com)