Source 1primary paper2020Journal of Cellular Physiology
Toolkit/MALAT1
MALAT1
Taxonomy: Mechanism Branch / Component. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
MALAT1 is a long noncoding RNA reported in trophoblasts to promote cell migration and invasion by reducing CRY2 protein abundance. In the cited study, MALAT1 recruits the E3 ubiquitin ligase FBXW7, impairing CRY2 protein stability and inducing ubiquitin-mediated CRY2 degradation.
Usefulness & Problems
Why this is useful
This RNA element is useful as a mechanistic regulator linking a lncRNA to post-translational control of CRY2 in trophoblast biology. It provides a reported means to modulate trophoblast migration and invasion through FBXW7-dependent protein degradation.
Source:
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Problem solved
The cited work addresses how MALAT1 can influence trophoblast migration and invasion at the molecular level. Specifically, it proposes that MALAT1 solves this regulatory task by recruiting FBXW7 to destabilize CRY2 and promote its ubiquitin-mediated degradation.
Problem links
Need conditional protein clearance
DerivedMALAT1 is a long noncoding RNA reported in trophoblasts to promote cell migration and invasion by reducing CRY2 protein abundance. In the cited study, MALAT1 recruits the E3 ubiquitin ligase FBXW7, impairing CRY2 protein stability and inducing ubiquitin-mediated CRY2 degradation.
Need conditional recombination or state switching
DerivedMALAT1 is a long noncoding RNA reported in trophoblasts to promote cell migration and invasion by reducing CRY2 protein abundance. In the cited study, MALAT1 recruits the E3 ubiquitin ligase FBXW7, impairing CRY2 protein stability and inducing ubiquitin-mediated CRY2 degradation.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Component: A low-level RNA part used inside a larger architecture that realizes a mechanism.
Mechanisms
Degradatione3 ligase recruitmentnegative regulation of protein stabilityubiquitin-mediated protein degradationTechniques
No technique tags yet.
Target processes
degradationrecombinationImplementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationoperating role: regulatorswitch architecture: recruitment
Practical implementation details are sparse in the supplied evidence. What is known is that the reported activity depends on endogenous or introduced MALAT1 acting in a context where FBXW7 and CRY2 are present, but no construct design, delivery method, expression system, or cofactor requirements are described here.
Evidence is limited to a single cited study in trophoblast and villous specimen contexts, with no independent replication provided here. The supplied evidence does not define sequence features, structural determinants, portability to other systems, or any role in recombination despite that target process being listed.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Observations
successMammalian Cell Lineapplication demotrophoblast
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
successMammalian Cell Lineapplication demotrophoblast
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
successMammalian Cell Lineapplication demotrophoblast
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
successMammalian Cell Lineapplication demotrophoblast
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
successMammalian Cell Lineapplication demotrophoblast
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
successMammalian Cell Lineapplication demotrophoblast
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
successMammalian Cell Lineapplication demotrophoblast
Inferred from claim c2 during normalization. MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. Derived from claim c2. Quoted text: MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
Supporting Sources
Ranked Claims
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
Approval Evidence
1 source5 linked approval claimsfirst-pass slug malat1
MALAT1
Source:
disease associationsupports
MALAT1 downregulation in trophoblasts might be related to miscarriage.
MALAT1 downregulation in trophoblasts might be related to miscarriage.
Source:
expression changesupports
MALAT1 expression is decreased in villous specimens from recurrent spontaneous abortion patients relative to missed abortion patients and normal villous specimens.
The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens.
Source:
functional effectsupports
MALAT1 promotes trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression.
Source:
molecular mechanismsupports
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation.
MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin-mediated degradation
Source:
molecular mechanismsupports
MALAT1 recruits FBXW7 to impair CRY2 protein stability.
MALAT1 recruited FBXW7 to impair CRY2 protein stability.
Source:
Comparisons
Source-backed strengths
The available evidence specifies a named substrate-ligase axis, FBXW7-CRY2, rather than only a correlative phenotype. The study also connects this mechanism to a cellular outcome, reporting that MALAT1 promotes trophoblast migration and invasion and is decreased in villous specimens from recurrent spontaneous abortion patients.
Compared with Cas6 binding site
MALAT1 and Cas6 binding site address a similar problem space because they share degradation, recombination.
Shared frame: same top-level item type; shared target processes: degradation, recombination; shared mechanisms: degradation
Compared with lipid nanoparticles
MALAT1 and lipid nanoparticles address a similar problem space because they share degradation, recombination.
Shared frame: shared target processes: degradation, recombination; shared mechanisms: degradation
Strengths here: may avoid an exogenous cofactor requirement.
Relative tradeoffs: appears more independently replicated.
Compared with synthetically engineered guide RNA
MALAT1 and synthetically engineered guide RNA address a similar problem space because they share degradation, recombination.
Shared frame: same top-level item type; shared target processes: degradation, recombination; shared mechanisms: degradation
Ranked Citations
- 1.